General Viral Bacterial Other
Health Conditions
Author(s):
Marshall
GD Jr ; Agarwal
SK
Affiliation: Division of Allergy and Clinical Immunology, University of
Texas Houston Medical School, Houston, USA.
Title: Stress,
immune regulation, and immunity: applications for asthma. Source: Allergy Asthma Proc (Allergy and asthma proceedings
: the official journal of regional and state allergy societies.) 2000
Jul-Aug; 21(4): 241-6
Abstract: The neuroendocrine mediators reach the cells of the immune system either through the peripheral circulation or through direct innervation of lymphoid organs. Primary and secondary lymphoid organs are innervated by sympathetic nerve fibers. Lymphocytes and monocytes express receptors for several stress hormones, including CRH, ACTH, cortisol, norepinephrine, and epinephrine. Therefore, it is reasonable to conclude that the neuroendocrine hormones released during a stressful event could alter immune function and subsequently alter the course of immune-based diseases. The impact of psychological stress on immune function has been the subject of extensive research efforts. Using a variety of models from largely healthy humans undergoing various forms of natural and experimental stress models, stress has been associated with suppression of NK activity, mitogen- and antigen-induced lymphocyte proliferation and in vitro production of IL-2 and IFN-gamma. Psychological stress is also associated with a higher rate of in vivo hypoergy to common recall-delayed type hypersensitivity antigens. These studies have suggested that psychological stress suppresses various components of CMI responses. Also, data suggest that chronic stress does not simply suppress the immune system, but induces a shift in the type-1/type-2 cytokine balance toward a predominant type-2 cytokine response. Such a change would favor the inflammatory milieu characteristic of asthma and allergic diseases. Recent studies using well-controlled teenage asthmatic subjects demonstrated immunological changes (decreased NK cell cytotoxicity and cytokine alterations) in response to exam stress. These immune alterations are consistent with a cytokine milieu that could potentially worsen asthma. However, there were no changes in peak flow rates, self-report asthma symptoms, or medication use. The lack of correlation between stress and asthma symptoms may have been related to the timing of the visits in relation to the stressor, the duration of the stressor, disease severity, or a lack of accurate self-report data. Alternatively, stress-mediated exacerbations of asthma may require multiple alterations by stress, including cytokine dysregulation or vagal-mediated airway hyperresponsiveness. The rationale for stress management in asthma is based upon the notion that stress causes a change in immune balance that would favor asthma activity in susceptible individuals. This immune imbalance can be found in TH1/TH2 cytokine changes that occur with stress. Although it has not yet been demonstrated that stress can cause or directly influence the development of asthma, it is interesting to note that both the incidence and prevalence of asthma continue to increase and are higher in urban than in rural areas. Among other differences is the well-appreciated higher chronic stress levels associated with urban living.
General Viral Bacterial Other Health Conditions
Author(s):
Gern
JE ; Busse
WW
Affiliation: Department of Pediatrics, University of Wisconsin Medical
School, Madison, USA.
Title: The role of
viral infections in the natural history of asthma. Source: J Allergy Clin Immunol (The Journal of allergy and
clinical immunology.) 2000 Aug; 106(2): 201-12
Abstract: Viral infections have been related to the inception of recurrent
wheezing illnesses and asthma in infants and are probably the most frequent
cause of exacerbations of established disease in older children and adults. The
well-recognized clinical effects of viral infections are mainly caused by
virus-induced immune responses. Clinical studies of natural and experimentally
induced viral infections have led to the identification of mechanisms of
inflammation that could be involved in producing airway obstruction and lower
airway symptoms. In addition, host factors that are associated with more
vigorous viral replication or severe clinical illness are beginning to be
identified. Advances in molecular virology and our understanding of immune
responses to viral infections may lead to the development of new strategies for
the prevention and treatment of virus-induced respiratory disorders.
Author(s):
Gern
JE ; Lemanske
RF Jr
Affiliation: Department of Pediatrics, University of Wisconsin Medical
School, Madison, WI 53792, USA. gern@medicine.wisc.edu Title: Infectious triggers of pediatric asthma. Source: Pediatr Clin North Am (Pediatric clinics of North
America.) 2003 Jun; 50(3): 555-75, vi
Abstract: Respiratory infections can cause wheezing illnesses in children of all
ages and also can influence the causation and disease activity of asthma. For
years it has been recognized that respiratory syncytial virus infections often
produce the first episode of wheezing in children who go on to develop chronic
asthma. More recently, it has been proposed that repeated infections with other
common childhood viral pathogens might help the immune system develop in such a
way as to prevent the onset of allergic diseases and possibly asthma. In
addition to the effects of viral infections, infections with certain
intracellular pathogens, such as chlamydia and mycoplasma, may cause acute and
chronic wheezing in some individuals, whereas common cold and acute sinus
infections can trigger acute symptoms of asthma. In this article, the
epidemiologic, mechanistic, and treatment implications of the association
between respiratory infections and asthma are discussed.
Author(s):
Yamaya
M ; Sasaki
H
Affiliation: Department of Geriatric and Respiratory Medicine, Tohoku University
School of Medicine, Sendai, Japan. yamaya@geriat.med.tohoku.ac.jp
Title: Rhinovirus
and asthma. Source: Viral Immunol
(Viral immunology.) 2003; 16(2): 99-109
Abstract: Rhinoviruses (RVs) cause the majority of common colds, which often
provoke wheezing in patients with asthma. The precise mechanisms responsible
for the RV infection-induced exacerbations of bronchial asthma are still
uncertain. However, several reports reveal airway hyperresponsiveness,
increases in chemical mediators in airway secretions such as kinin and
histamine, and airway inflammation in patients with bronchial asthma after RV
infection. RV infection induces an accumulation of inflammatory cells in airway
mucosa and submucosa including neutrophils, lymphocytes and eosinophils. RV
affects the barrier function of airway epithelial cells, and activates the
airway epithelial cells and other cells in the lung to produce pro-inflammatory
cytokines, including various kinds of interleukins, GM-CSF and RANTES, and
histamine. RV also stimulates the expression of intercellular adhesion
molecule-1 (ICAM-1) and low-density lipoprotein receptors in the airway
epithelium, receptors for major and minor RVs. On the other hand, RV infection
is inhibited by treatment with soluble ICAM-1, and by reduction of ICAM-1
expression in the airway epithelial cells after treatment with erythromycin.
Both soluble ICAM-1 and erythromycin were reported to reduce the frequency of
common colds. Here, we review the pathogenesis and management of RV infection-induced
exacerbation of bronchial asthma.
Author(s):
Jacoby
DB
Affiliation: Johns Hopkins School of Public Health, 615 N Wolfe St, Room
W7006, Baltimore, MD 21205, USA. djacoby@jhmi.edu Title: Virus-induced asthma attacks. Source: JAMA (JAMA : the journal of the
American Medical Association.) 2002 Feb 13; 287(6): 755-61
Abstract: Viral respiratory tract infections are a common cause of asthma attacks.
Study of this phenomenon has revealed multiple mechanisms and contributed to
understanding of the increase in airway inflammation and bronchoconstriction
observed in this context. Changes in the neural control of the airways
contribute to bronchoconstriction, which is reflected in an increased efficacy
of anticholinergic medications during acute asthma attacks. The ability to
prevent or treat viral respiratory tract infections is currently limited.
However, as more effective antiviral treatments and vaccines become available,
such therapies are likely to be effective in patients with asthma. Clinical
management of this problem is illustrated in this article by the case of a
40-year-old woman with history of mild asthma who was admitted to an intensive
care unit with severe bronchospasm and an upper respiratory tract infection.
Author(s):
Welliver
RC
Affiliation: Department of Pediatrics, State University of New York at
Buffalo, The Children's Hospital of Buffalo, USA.
Title: Immunologic
mechanisms of virus-induced wheezing and asthma. Source: J Pediatr (The Journal of pediatrics.)
1999 Aug; 135(2) Pt 2: 14-20
Abstract: Viral infections are a common cause of wheezing at all ages. In
addition, it has been suggested that viral infections can induce a long-term
asthma diathesis. Because asthma is increasingly understood to be an
inflammatory disease, there is great interest in the immunologic mechanisms
that may underlie virus-induced wheezing. Viral infections may induce
inflammatory responses that closely resemble those characteristic of asthma,
including airway infiltration with lymphocytes and eosinophils and release of
mediators of airway obstruction. Certain viruses preferentially enhance pre-existing
inflammatory responses in atopic individuals. Alternatively, viral infections
may induce an altered reactivity favoring the expression of atopy. Finally,
immunologic responses to viral infections may serve only as markers of the
subsequent development of atopy.
Author(s):
Grünberg
K ; Sterk
PJ
Affiliation: Department of Pulmonology, Leiden University Medical
Center, The Netherlands.
Title: Rhinovirus
infections: induction and modulation of airways inflammation in asthma.
Source:
Clin Exp Allergy (Clinical and experimental allergy
: journal of the British Society for Allergy and Clinical Immunology.) 1999
Jun; 29 Suppl 2: 65-73
Abstract: There is renewed interest in the role of respiratory virus infections in
the pathogenesis of asthma and in the development of exacerbations in
pre-existing disease. This is due to the availability of new molecular and
experimental tools. Circumstantial evidence points towards a potentially
causative role as well as to possibly protective effects of certain respiratory
viruses in the cause of allergic asthma during early childhood. In addition, it
now has become clear that exacerbations of asthma, in children as well as
adults, are mostly associated with respiratory virus infections, with a
predominant role of the common cold virus: rhinovirus. Careful human in vitro
and in vivo experiments have shown that rhinovirus can potentially stimulate
bronchial epithelial cells to produce pro-inflammatory chemokines and
cytokines, may activate cholinergic- or noncholinergic nerves, increase
epithelial-derived nitric oxide synthesis, upregulate local ICAM-1 expression,
and can lead to nonspecific T-cell responses and/or virus-specific T-cell
proliferation. Experimental rhinovirus infections in patients with asthma
demonstrate features of exacerbation, such as lower airway symptoms, variable
airways obstruction, and bronchial hyperresponsiveness, the latter being
associated with eosinophil counts and eosinophilic cationic protein levels in
induced sputum. This suggests that multiple cellular pathways can be involved
in rhinovirus-induced asthma exacerbations. It is still unknown whether these
mechanisms are a distinguishing characteristic of asthma. Because of the
limited effects of inhaled steroids during asthma exacerbations, new
therapeutic interventions need to be developed based on the increasing
pathophysiological knowledge about the role of viruses in asthma.
Author(s):
Macek
V ; Dakhama
A ; Hogg
JC ; Green
FH ; Rubin
BK ; Hegele
RG
Affiliation: McDonald Research Laboratories, St Paul's Hospital,
Vancouver, Canada.
Title: PCR
detection of viral nucleic acid in fatal asthma: is the lower respiratory tract
a reservoir for common viruses? Source: Can Respir J (Canadian respiratory journal : journal of the Canadian
Thoracic Society.) 1999 Jan-Feb; 6(1): 37-43
Abstract: BACKGROUND: There is indirect evidence implicating viral respiratory
tract infections in the pathogenesis of fatal asthma. However, it is unknown
whether viruses are present within the lower respiratory tract in fatal asthma.
OBJECTIVES: To apply a nine-virus polymerase chain reaction (PCR) panel to
postmortem specimens of lower airway secretions and compare the prevalence of
viral nucleic acid among patients who died of asthma, asthmatic patients who
died of other causes and persons who died without lung disease. PATIENTS AND
METHODS: Postmortem specimens of lower airway secretions from patients who died
of asthma (fatal asthma [n=10]), asthmatic patients who died of other causes
(n=4) and nonasthma controls (n=6) underwent PCR for nine common respiratory viruses.
The prevalence of each virus was compared among the three groups. RESULTS: PCR
was positive for at least one virus in 19 of 20 cases, and multiple viruses
were detected in 14 of 20 cases. The prevalence of each virus was similar in
the three groups studied. CONCLUSIONS: In fatal asthma, lower airway secretions
do not show a specific pattern of viral nucleic acid. Intriguingly, these
results suggest that the lower respiratory tract may act as a potential
reservoir for common respiratory viruses.
Author(s):
Isaacs
D ; Joshi
P
Affiliation: Department of Immunology and Infectious Diseases, The
Children's Hospital at Westmead, University of Sydney, NSW. davidi@chw.edu.au
Title: Respiratory
infections and asthma. Source: Med J Aust (The Medical journal of Australia.) 2002 Sep 16; 177
Suppl: S50-1
Abstract: What we know: Respiratory viral infections caused by rhinoviruses, coronaviruses, influenza, parainfluenza and respiratory syncytial viruses (RSVs) are important triggers of asthma attacks. Mycoplasma and Chlamydia infections can also provoke asthma attacks, although less commonly. RSV infections probably do not cause asthma, but are potent triggers of wheezing, with the result that RSV infection often reveals underlying asthma in children. RSV infection does not cause atopy. Bacterial respiratory infections in infancy appear to protect against later atopy. What we need to know: Does RSV infection in infancy alter a child's T(H)1/T(H)2 responses to later infections with other respiratory pathogens? What are the mechanisms (immunological or mechanical) by which respiratory pathogens cause wheezing? What is the role of respiratory infections in exacerbations of asthma? Can epidemiology shed light on this? Do viruses such as RSV cause asthma or uncover underlying asthma? Do children respond differently to RSV than to other viruses? Does atopy affect those responses? Do bacterial respiratory infections truly protect against future atopy?
Author(s): Van
Bever HP ; Chng
SY ; Goh
DY
Affiliation: Pediatric Allergy and Immunology Division, National
University of Singapore, Singapore.
Title: Childhood severe acute respiratory syndrome, coronavirus infections and asthma.
Source: Pediatr Allergy Immunol (Pediatric allergy and immunology : official publication
of the European Society of Pediatric Allergy and Immunology.) 2004 Jun;
15(3): 206-9
Abstract: Van Bever HP, Chng SY, Goh DY. Childhood severe acute respiratory
syndrome, coronavirus infections and asthma. Pediatr Allergy Immunol 2004: 15:
206-209.
Copyright 2004 Blackwell MunksgaardSevere acute respiratory syndrome (SARS) is
a new infectious disease caused by a novel coronavirus. Children appear to be
less susceptible to the SARS coronavirus, although the other non-SARS coronaviruses
can cause respiratory infections in adults and in children of all ages. The
exact reasons as to why SARS preferentially affects adults, and not children,
are still unknown. Many hypotheses exist and need to be explored. During the
outbreak of SARS, there did not appear to be an increase in asthma
exacerbations in children.
Author(s):
Schwarze
J ; Schauer
U
Affiliation: Children's Clinic, St Josef-Hospital, 44791 Bochum,
Germany. j.schwarze@ic.ac.uk
Title: Enhanced
virulence, airway inflammation and impaired lung function induced by
respiratory syncytial virus deficient in secreted G protein. Source: Thorax (Thorax.) 2004 Jun; 59(6):
517-21
Abstract:
BACKGROUND: Respiratory
syncytial virus (RSV) infection can cause bronchial hyperresponsiveness and
asthma exacerbations. In mice it results in airway inflammation and airway
hyperresponsiveness. Since viral factors influencing these responses are not
well defined, a study was undertaken to investigate the role of secreted G
protein of human RSV in determining virulence, inflammatory responses, and changes
in lung function. METHODS: BALB/c mice were infected with a spontaneous mutant
of RSV deficient in secreted G protein (RSV-DeltasG) or with wild type RSV
(RSV-WT). Viral titres, numbers of pulmonary inflammatory cells, and
concentrations of interferon (IFN)-gamma, interleukin (IL)-4, IL-5 and IL-10 in
bronchoalveolar lavage (BAL) fluid were determined. Airway function was
assessed at baseline and following methacholine provocation using barometric
whole body plethysmography. RESULT: Following infection with RSV-DeltasG, viral
titres were increased 50-fold compared with RSV-WT. Influx of eosinophils and
macrophages to the lung and concentrations of IFN-gamma and IL-10 in BAL fluid
were also significantly higher following infection with RSV-DeltasG. Airway function,
both at baseline and after methacholine provocation, was significantly
decreased following infection with RSV-DeltasG compared with RSV-WT.
CONCLUSION: Secreted G protein is likely to be a regulatory factor in RSV
infection limiting infectivity of the virus, inflammatory responses in the
lungs, and reduction in lung function.
Author(s):
Lee
AM ; Fryer
AD ; van
Rooijen N ; Jacoby
DB
Affiliation: Division of Pulmonary and Critical Care Medicine, Johns
Hopkins University, Baltimore, Maryland 21205, USA.
Title: Role of
macrophages in virus-induced airway hyperresponsiveness and neuronal M2 muscarinic
receptor dysfunction. Source: Am J Physiol Lung Cell Mol Physiol (American journal of physiology.
Lung cellular and molecular physiology.) 2004 Jun; 286(6): L1255-9
Abstract: Viral infections exacerbate asthma. One of the pathways by which viruses
trigger bronchoconstriction and hyperresponsiveness is by causing dysfunction
of inhibitory M(2) muscarinic receptors on the airway parasympathetic nerves.
These receptors normally limit acetylcholine (ACh) release from the
parasympathetic nerves. Loss of M(2) receptor function increases ACh release,
thereby increasing vagally mediated bronchoconstriction. Because viral
infection causes an influx of macrophages into the lungs, we tested the role of
macrophages in virus-induced airway hyperresponsiveness and M(2) receptor
dysfunction. Guinea pigs infected with parainfluenza virus were hyperresponsive
to electrical stimulation of the vagus nerves but not to intravenous ACh,
indicating that hyperresponsiveness was due to increased release of ACh from
the nerves. In addition, the muscarinic agonist pilocarpine no longer inhibited
vagally induced bronchoconstriction, indicating M(2) receptor dysfunction.
Treating animals with liposome-encapsulated dichloromethylene-diphosphonate
depleted macrophages as assessed histologically. In these animals, viral
infection did not cause airway hyperresponsiveness or M(2) receptor
dysfunction. These data suggest that macrophages mediate virus-induced M(2)
receptor dysfunction and airway hyperresponsiveness.
Author(s):
Akazawa
S ; Matsuse
H ; Saeki
S ; Machida
I ; Kondo
Y ; Tsuchida
T ; Kohno
S
Affiliation: Second Department of Internal Medicine, Nagasaki University
School of Medicine, 1-7-1 Sakamoto, Nagasaki 852-8501, Japan.
Title: [Two cases
of asthmatic exacerbation caused by parainfluenza virus 3 infection]
Source:
Nihon Kokyuki Gakkai Zasshi (Nihon Kokyuki Gakkai zasshi =
the journal of the Japanese Respiratory Society.) 2004 Apr; 42(4): 353-6
Abstract: Although viral respiratory tract infections are considered to be the
most frequent causes of asthmatic exacerbation, respiratory viruses can rarely
be detected in the adult population. We describe 2 cases, in a 43-yr-old man
with severe atopic asthma and in a 69-yr-old man with moderate non-atopic
asthma. After the onset of nasal discharge, sore throat and fever, the asthma
had become exacerbated in both cases during the summer of 2002. In both cases,
parainfluenza virus (PIV) 3 viral RNA could be detected from oral gargling by
RT-PCR, and the serum viral antibody titer against PIV 3 increased
significantly. These cases were therefore diagnosed as undergoing asthmatic
exacerbation caused by PIV 3 infection and were successfully treated with
systemic steroids. During summer, 2002, in our outpatient clinic, PIV 3
infection was demonstrated in approximately half of the asthmatic exacerbations
associated with upper respiratory symptoms, including the present cases.
Collectively, PIV 3 seems to represent an important viral cause of asthma
exacerbation in summer.
Author(s): Peebles
RS Jr
Affiliation: Division of Allergy, Pulmonary, and Critical Care Medicine,
Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2650, USA.
Title: Viral
infections, atopy, and asthma: is there a causal relationship? Source: J Allergy Clin Immunol (The Journal of allergy and
clinical immunology.) 2004 Jan; 113(1) Suppl: S15-8
Abstract: Respiratory syncytial virus (RSV) remains the chief cause of
hospitalization for lower respiratory tract illnesses in both infants and young
children, and can produce severe outcomes. In addition, several studies have
suggested that infants in whom RSV bronchiolitis develops may have recurrent
wheezing and asthma later in childhood. Further complicating the picture is the
question of whether there is a link between RSV infection in infancy and the
development of atopy later in childhood. This review will discuss existing data
on RSV infection and respiratory complications later in life, as well as the
link between RSV and allergic disease.
Author(s):
Peebles
RS Jr ; Hartert
TV
Affiliation: Department of Medicine, Vanderbilt University School of
Medicine, Nashville, TN 37232-2650, USA.
Title: Respiratory
viruses and asthma. Source: Curr Opin Pulm Med (Current opinion in pulmonary medicine.) 2000 Jan;
6(1): 10-4
Abstract: Viral infections have become increasingly recognized as a significant
cause of asthma exacerbations, mainly because of improved viral detection
techniques. Unfortunately, the ability to specifically treat viral infections
and to limit the asthma morbidity associated with these agents has not kept
pace with diagnostic technology. This article focuses on current concepts of
the epidemiology of viruses in asthma exacerbations, investigations studying
the physiologic and immunologic consequences of viral infection, and potential
therapies to minimize virally-induced airway hyperresponsiveness. To impact
this significant health problem, researchers must definitively ascertain the
mechanisms by which viruses induce airway reactivity and must develop rational,
safe approaches to prevent the consequences of viral infection in the patient
with asthma.
Author(s):
Hogg
JC
Affiliation: UBC Pulmonary Research Laboratory, St. Paul's Hospital,
Vancouver, British Columbia, Canada. uhogg@mrl.ubc.ca Title: Childhood viral infection and the pathogenesis of
asthma and chronic obstructive lung disease. Source: Am J Respir Crit Care Med (American journal of respiratory
and critical care medicine.) 1999 Nov; 160(5) Pt 2: S26-8
Abstract: Many epidemiologic studies have implicated childhood respiratory infections
as an independent risk factor for the subsequent development of persistent
asthma and chronic obstructive pulmonary disease (COPD). The majority of these
childhood infections are viral in origin, and great strides are being made in
understanding their pathogenesis at the molecular level. Some viruses, such as
respiratory syncytial virus-a common cause of childhood bronchiolitis-stimulate
the helper T cell type 2 (Th2) pattern of immune responses associated with
allergic inflammation. Other viruses, such as adenovirus, appear to persist as
latent infections in the airways of patients with COPD, and adenoviral E1A
protein is capable of amplifying host genes, possibly including those involved
in cigarette smoke-induced lung inflammation. Studies of the chronic, low-grade
peripheral lung inflammation caused by adenoviral infection of guinea pigs will
enable examination of the possibility that latent infection may induce
resistance to the antiinflammatory actions of corticosteroids. Studies of the
molecular mechanisms of viral infections of the airways could provide important
insights into the nature of the inflammatory process involved in asthma and
COPD. Hogg JC. Childhood viral infection and the pathogenesis of asthma and
chronic obstructive lung disease.
Author(s):
Allegra
L ; Blasi
F ; Centanni
S ; Cosentini
R ; Denti
F ; Raccanelli
R ; Tarsia
P ; Valenti
V
Affiliation: Institute of Respiratory Diseases, University of Milan,
Italy.
Title: Acute
exacerbations of asthma in adults: role of Chlamydia pneumoniae infection.
Source:
Eur Respir J (The European respiratory
journal : official journal of the European Society for Clinical Respiratory
Physiology.) 1994 Dec; 7(12): 2165-8
Abstract: Respiratory infections precipitate wheezing in many asthmatic patients
and may be involved in the aetiopathogenesis of asthma. Several studies have
demonstrated that viral infections may provoke asthma. Bacterial infections
seem to play a minor role. However, Chlamydia pneumoniae has been recently
reported as a possible cause of asthma. The aim of the present study was to
evaluate the role of C. pneumoniae infection in acute exacerbations of asthma
in adults. Seventy four adult out-patients with a diagnosis of acute
exacerbation of asthma were studied. Acute and convalescent (> or = 3 weeks)
serological determination of antibodies to cytomegalovirus, respiratory
syncytial virus, adenovirus, influenza A and B, parainfluenza 1 and 3,
Mycoplasma pneumoniae and Legionella pneumophila were performed by means of
immunofluorescence tests. C. pneumoniae specific antibodies were detected by
two microimmunofluorescence tests using a specific antigen (TW-183) and a kit
with three chlamydial antigens. Pharyngeal swab specimens were also obtained
for C. pneumoniae identification. Samples for bacterial culture were obtained
in patients with productive cough (15 out of 74 patients). Fifteen patients
(20%) presented seroconversion to at least one of the studied pathogens. Seven
were found to be infected by virus, six by C. pneumoniae alone, and one by M.
pneumoniae. One more patient showed seroconversion to C. pneumoniae and
cytomegalovirus.(ABSTRACT TRUNCATED AT 250 WORDS)
Author(s):
von
HL
Affiliation: The Finnish Lung Health Association, Helsinki.
leena.vonhertzen@filha.fi
Title: Role of
persistent infection in the control and severity of asthma: focus on Chlamydia
pneumoniae. Source: Eur Respir J
(The European respiratory journal : official journal of the European Society
for Clinical Respiratory Physiology.) 2002 Mar; 19(3): 546-56
Abstract: Conventional risk factors have been unable to explain most of the
substantial increase in the prevalence of asthma observed in many countries
during the last few decades. Much attention has been directed at the
"hygiene hypothesis", the apparent inverse relationship between
intense systemic childhood infections and the subsequent development of asthma
and atopy. However, it is not only the absence or scarcity of infections, but
the prolonged presence of certain microorganisms in the lungs that may be
involved in the development of asthma. Accumulating evidence suggests that
Chlamydia pneumoniae, an intracellular ubiquitous pathogen with an innate
propensity to persist and cause chronic infections, may be associated with
asthma. This microorganism can achieve a state of "latency" in which
it is viable but dormant and does not multiply. During this state, however,
chlamydia continues to synthesize the "stress" protein, a 60-kDa heat
shock protein (hsp60). This protein is able to elicit a strong host
inflammatory response at sites of its production and appears to be involved in
tissue injury and scarring processes. As inflammation has been found to be
present in almost all asthmatics, whatever the severity and aetiology of the
disease, inhaled glucocorticoids now have an established position in the
treatment of early stages. However, corticosteroids negatively affect many
aspects of cell-mediated immunity and favour the shift from a T-helper-1-type
response towards a T-helper-2-type response. Corticosteroids may thus severely
deteriorate the host's ability to eradicate an intracellular pathogen, such as
Chlamydia pneumoniae, which requires a properly functioning cell-mediated
(T-helper-1-type) immune response to be cleared. These drugs are also able to
reactivate persistent Chlamydia to an active growth phase, which, by increasing
the production of pro-inflammatory cytokines at the site of infection, can
further amplify inflammation in the airways of patients with asthma.
Author(s):
Gern
JE
Affiliation: Department of Pediatrics, University of Wisconsin-Madison,
Madison, Wisconsin 53792-9988, USA.
Title: Rhinovirus
respiratory infections and asthma. Source: Am J Med (The American journal of medicine.) 2002 Apr 22; 112
Suppl 6A: 19S-27S
Abstract: Viral infections, particularly respiratory illnesses caused by
rhinovirus, are the most common cause of asthma exacerbations in children and contribute
in large part to asthma morbidity in adults. Epidemiologic studies and
increasingly sophisticated viral detection methodologies have helped to define
the role of rhinovirus as a potential causative agent in asthma exacerbations.
Rhinovirus-induced lung disease is multifaceted and can be characterized in
terms of a variety of physiologic, immunologic, and viral processes. The
precise direct and indirect mechanisms of viral contribution to exacerbations
must still be elucidated. Understanding them will have an impact on the design
of future treatment modalities.
Author(s):
Martin
RJ ; Kraft
M ; Chu
HW ; Berns
EA ; Cassell
GH
Affiliation: Department of Medicine, National Jewish Medical and
Research Center and The Pulmonary and Critical Care Division, University of
Colorado Health Sciences Center, 1400 Jackson St., Denver, CO 80206, USA.
Title: A link
between chronic asthma and chronic infection. Source: J Allergy Clin Immunol (The Journal of allergy and
clinical immunology.) 2001 Apr; 107(4): 595-601
Abstract: BACKGROUND: Asthma is a prevalent
disease with marked effects on quality of life and economic societal burden.
However, the cause of asthma and its pathophysiology are not completely
defined. Recently, the possibility that chronic infection may play a role has
been suggested. OBJECTIVE: We sought to define the association between
Mycoplasma and Chlamydia species and chronic asthma. METHODS: We performed a
comparison study of asthmatic patients and normal control subjects. Fifty-five
patients with chronic stable asthma were compared with 11 normal control
subjects by using PCR, culture, and serology for Mycoplasma species, Chlamydia
species, and viruses from the nasopharynx, lung, and blood. Bronchoalveolar
lavage cell count and differential, as well as tissue morphometry, were also
evaluated. Computer-generated scoring for the degree of chronic sinusitis in
asthmatic patients was additionally evaluated. RESULTS: Thirty-one of 55
asthmatic patients had positive PCR results for Mycoplasma (n = 25) or
Chlamydia species (n = 6), which were mainly found on lung biopsy specimens or
in lavage fluid. Only 1 of 11 normal control subjects had positive PCR results
for Mycoplasma species. The distinguishing phenotype between asthmatic patients
with positive and negative PCR results was the significantly greater number of
tissue mast cells in the group with positive results. CONCLUSION: A significant
number of patients with chronic stable asthma demonstrate the presence of
Mycoplasma species, Chlamydia species, or both in their airways, with the
distinguishing feature of increased mast cell number. These findings need
further delineation but may help us to understand the pathophysiology of asthma
and new treatment options.
Author(s):
Mygind
N
Affiliation: Dept of Respiratory Diseases, University Hospital of
Aarhus, DK-8000 Aarhus, Denmark.
Title: The common
cold as a trigger of asthma. Source: Monaldi Arch Chest Dis (Monaldi archives for chest
disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del
lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato
respiratorio, Universita di Napoli, Secondo ateneo.) 2000 Dec; 55(6):
478-83
Abstract: The common cold is a viral disease with predominant symptoms from the upper airways. Rhinovirus is the most important common cold virus, and rhinovirus infection is predominantly transmitted by direct contact (nasal secretion-hand (object)-hand-mucous membrane in eye and nose). The viral disease results in the release of IL-8 from nasal epithelial cells, causing a neutrophil-dominated inflammation in the nose. The biochemical mediators, causing nasal symptoms, have not yet been identified. A common cold is the most important cause of exacerbations of asthma in children and also in adults. The rhinovirus infection induces airway inflammation, bronchial hyperresponsiveness and asthma symptoms. However, the mode of action of the virus-induced inflammation on the asthma disease is poorly understood. As a routine, physicians give oral corticosteroid and increase the dosage of inhaled corticosteroid during a common cold-induced exacerbation of asthma, but there do not seem to be any placebo-controlled trials in support of this practice.
General Viral Bacterial Other Health Conditions
Author(s):
Kraft
M
Affiliation: Department of Medicine, National Jewish Medical and
Research Center, University of Colorado Health Sciences Center, Denver, USA.
kraftm@njc.org
Title: The role of
bacterial infections in asthma. Source: Clin Chest Med (Clinics in chest medicine.) 2000 Jun; 21(2): 301-13
Abstract: In summary, bacterial organisms are clinically relevant contributors to
asthma exacerbations, and have received much less attention than viruses in
this process. Streptococcus pneumoniae, Hemophilus influenzae, and Moraxella
catarrhalis have been linked to asthma exacerbations, particularly when
sinusitis is present. Treatment therefore should be directed toward these
organisms if a bacterial cause is suspected. The atypical
bacteria--specifically, C. pneumoniae and M. pneumoniae--deserve special
attention. Data suggest a link between these organisms and the exacerbation of
asthma, as well as suggest that these organisms may be causative in asthma
development. The existing data are not conclusive, but are suggestive enough to
drive studies evaluating them as a possible mechanism in asthma pathogenesis.
An animal model evaluating M. pneumoniae and C. pneumoniae would be ideal, but
at present no model exists in which chronic infection with these organisms
results in bronchial hyperresponsiveness. There is active work in this area,
however. Alternative investigations include continued evaluation of these
organisms by several modalities, including culture, serology, and PCR, along
with evaluation of the host response. Many questions remain, but the ground is
fertile for continued investigation.
Author(s):
Virant
FS
Affiliation: Northwest Asthma & Allergy Center, University of
Washington, 4540 Sand Point Way NE, Seattle, WA 98105, USA.
fvirant@nwasthma.com
Title: Sinusitis
and asthma: associated airway diseases. Source: Curr Allergy Asthma Rep (Current allergy and asthma
reports.) 2001 May; 1(3): 277-81
Abstract: Sinusitis and asthma often coexist in patients. In fact, these airways
disorders are similar histologically, with tissue eosinophils, increased
glandular tissue, and edema. Medical or surgical therapy for sinusitis often
greatly improves asthma, suggesting that sinusitis may exacerbate asthma.
Possible mechanisms by which asthma could be worsened by sinus disease include
neural reflex pathways and interference with the important nasal functions of
heating, humidification, and filtration. Health professionals treating
asthmatic patients should consider sinusitis as a possible underlying cause, in
addition to other triggers (e.g., allergic rhinitis and gastroesophageal reflux
disease).
Author(s):
Gern
JE
Affiliation: University of Wisconsin Medical School, Madison, Wisconsin,
USA. Title:
Viral and bacterial infections in the
development and progression of asthma. Source: J Allergy Clin Immunol (The Journal of allergy and
clinical immunology.) 2000 Feb; 105(2) Pt 2: S497-502
Additional Info: UNITED STATES Standard No: ISSN: 0091-6749; NLM Unique Journal
Identifier: 1275002 Language: English Abstract: Viral respiratory infections produce wheezing illnesses in
patients of all ages. In infancy, infections with respiratory syncytial virus
and parainfluenza virus are the major cause of bronchiolitis and croup, whereas
infections with common cold viruses such as rhinoviruses are the principal
triggers for wheezing in older children and adults with asthma. In addition to
causing increased wheezing in asthma, there is mounting evidence that
infections early in childhood can affect the development of the immune system
and thereby modify the risk for the subsequent development of allergies and
asthma. Both of these effects appear to be mediated by virus-induced immune
responses. Early during the course of viral infection, resident cells in the
airway are activated in an antigen-independent fashion, triggering antiviral
responses but also activating and recruiting cells to the airway that could
contribute to airway obstruction and respiratory symptoms. Virus-specific T-
and B-cell responses may also have dual effects in the presence of preexisting
airway inflammation. Finally, there is evidence of synergistic interactions
between allergen- and virus-induced airway inflammation. It is likely that
greater definition of mechanisms of virus-induced inflammation will provide
therapeutic targets for the treatment and possibly the prevention of allergies
and asthma.
General Viral Bacterial Other
Health Conditions
Affiliation: Veterans Affairs Hospital, Hines, Illinois 60141, USA.
Title: Gastroesophageal
reflux disease and asthma. Source: J Clin Gastroenterol (Journal of clinical
gastroenterology.) 2000 Apr; 30(3) Suppl: S9-30
Abstract: Gastroesophageal reflux (GER) and asthma occur together frequently. The relationship has been recognized for more than 2,000 years but has not been appreciated until recently. Attempts to determine the number of asthmatics that currently have GER (prevalence) have shown a higher-than-expected prevalence. Of the approximately 200 published studies on the relationship between GER and asthma, the true prevalence of GER in asthmatics, however, can be estimated from fewer than 20 of the studies. These studies, which comprise highly selected referred populations, are unlikely to reflect the overall population of patients with asthma. Nevertheless, the estimated prevalence of GER in asthmatics is between 60-80% in adults and 50-60% in children. No attempts have been made to determine the incidence of GER in asthmatics. To identify asthmatics who develop GER over time would be a formidable task, requiring decades of close follow-up of asthmatics who do not now have GER. Despite the lack of data on the incidence of GER, data on the prevalence raise an important issue: If the prevalence of GER in adult asthmatics is similar to the prevalence of GER in child asthmatics, what is the true incidence of GER? There are two potential answers: (1) all of the child asthmatics with GER grow up to become the adult asthmatics with GER (GER incidence = 0%); and (2) some child asthmatics with GER outgrow either the GER or the asthma; some adults with asthma develop GER while others with GER develop asthma (low, medium, or high incidence depending on the numbers). It is not unreasonable to suspect that some child asthmatics with GER become adult asthmatics with GER, and that children with GER who apparently "outgrow" their asthma surface later as adults with both asthma and GER. Because most children leave their pediatricians after adolescence, the information required to demonstrate continued asthma or GER is lost. As a result, the medical community sees two completely different populations, each with very similar conditions: childhood asthma with GER and adult asthma with GER. If the high prevalence of GER in asthmatics is clinically relevant, it should be readily explainable. We suggest that the GER/asthma relationship consists of a self-propagating situation whereby reflux aggravates asthma, which in turn induces further reflux. In the early course of the disease, asthma may not be apparent, as aspiration-induced pulmonary symptoms may occur very infrequently-perhaps once or twice a year. With time, however, aspiration may become more frequent, and the pulmonary tree may become hypersensitive. The individual may be diagnosed as having asthma. The pulmonary tree becomes increasingly hypersensitive, to a variety of stimuli. In such a scenario, the initial contribution of acid aspiration is no longer apparent, as the primary focus is on the asthma. In any individual patient, the emphasis may be placed on the GER if reflux symptoms predominate or on asthma if pulmonary symptoms predominate. The result is confusion over whether a patient with GER has asthma or whether a patient with asthma has GER. The unending debate about whether GER is a cause of the asthma or a result of the asthma becomes the focus of attention. At such a point, the question of whether GER exists in asthmatics or whether pulmonary symptoms exist in refluxers is irrelevant. For the individual patient, gastric contents refluxed into the pulmonary tree is an undesirable event, whether cause or effect, and it is up to the physician to determine how such events can be stopped.
Author(s):
Wasowska-Królikowska
K ; Toporowska-Kowalska
E ; Krogulska
A
Affiliation: Clinic of Pediatric Gastroenterology and Allergology,
Institute of Paediatrics, Medical University, Lódz, Poland.
Title: Asthma and
gastroesophageal reflux in children. Source: Med Sci Monit (Medical science monitor : international medical journal
of experimental and clinical research.) 2002 Mar; 8(3): RA64-71
Abstract: Gastroesophageal reflux (GER) is a factor often neglected in the
etiopathogenesis of asthma. The estimated incidence of GER in asthmatic
children reaches 50-60% and is higher than in the general population. GER may
accompany typical symptoms: hoarseness, sore throat, thoracic pain, cough or
wheezing. GER may not only aggravate the course of bronchial obstruction, but
may also cause it, or trigger obstruction due to other factors. Asthma and GER
coincidence has been acknowledged for many years. The paper presents a current
review of studies concerning the relations between asthma and GER and attempts
to establish, which is the cause and which is the result. The hypotheses how
GER can lead to bronchial obstruction, and how obstruction can aggravate GER,
are also presented. GER is believed to be a factor causing obstruction by: 1.
an indirect mechanism - reflex theory, 2. a direct mechanism - reflux theory,
and 3. a neuropeptide-mediated mechanism. The paper also presents diagnostic
methods allowing to detect GER in asthmatics. A review of recent studies
concerning the treatment of GER in asthmatics, both with pharmacological and
surgical methods, is also included. Beneficial effect of antireflux therapy on
the course of asthma has been emphasized. Therefore, antireflux therapy is
recommended in all patients with concurrent asthma and GER, irrespective of
severity of clinical GER symptoms, even in those with silent GER. The essential
drugs used in the treatment of GER are proton pump inhibitors. Appropriately
high dose level and appropriately long duration of the therapy should be taken
into consideration.
Author(s):
Anderson
SD
Affiliation: Department of Respiratory Medicine, Royal Prince Alfred
Hospital, Camperdown, NSW, Australia.
Title: Exercise-induced
asthma and the use of hypertonic saline aerosol as a bronchial challenge.
Source:
Respirology (Respirology (Carlton, Vic.))
1996 Sep; 1(3): 175-81
Abstract: Exercise induced asthma is a common complaint and the prevalence appears
to be increasing worldwide. Once confined to the research domain of university
teaching hospitals, the study of EIA has extended into the school playground,
defence force establishments and sports institutions. Standardized protocols
have been developed to study EIA in the laboratory and in the field. A
surrogate challenge using eucapnic or isocapnic hyperventilation with dry air
is becoming popular because it has advantages over exercise, at least for
adults. The stimulus that leads the airways to narrow is caused by the
inhalation of dry air during hyperventilation and exercise, during which water
is evaporated from the airways in order to condition the inspired air. The
mechanism whereby the airways narrow is thought to be due to the dehydrating
effects of water loss, particularly in relation to its potential to cause the
airways to become hyperosmolar. Mast cell mediators such as histamine and the
leucotrienes are probably involved in EIA because specific antagonists reduce
severity. As a result of the osmotic theory of EIA, studies were carried out to
determine whether subjects with EIA were sensitive to the effects of increasing
airway osmolarity by inhalation of hyperosmolar aerosols of sodium chloride. A
challenge protocol using an aerosol of 4.5% sodium chloride, generated from an
ultrasonic nebulizer, has been used to identify persons with asthma and to
assess response to drug therapy. There are many similarities between responses
to exercise, hyperventilation and hypertonic saline in the physiological and
biochemical responses and the responses to drugs. Challenge with hypertonic
saline is easier and cheaper to use because expensive equipment and a source of
dry air is not required as with exercise or hyperventilation. The ability to
obtain a dose-response curve rather than a single response and the ability to
collect inflammatory cells at the same time make challenge with hypertonic
saline an attractive technique to study patients suspected of having asthma.
Author(s):
D'Alonzo
GE ; Ciccolella
DE
Affiliation: Temple University Health Sciences Center, Philadelphia, PA
19140, USA.
Title: Nocturnal
asthma: physiologic determinants and current therapeutic approaches.
Source:
Curr Opin Pulm Med (Current opinion in pulmonary
medicine.) 1996 Jan; 2(1): 48-59
Abstract: Asthma has a tendency to destabilize at night in patients that are
diurnaly active and try to sleep at night. As asthma worsens, the expression of
this disease seems to increase at night. Additionally, nocturnal asthmatics
have increased airway hyperresponsiveness and likely more active inflammation
at night as compared with the daytime. Although the cause of nocturnal asthma
cannot be completely explained, there do appear to be a variety of internal body
circadian rhythms that play a role in this disease. Also, noncircadian rhythmic
influences such as sleep, supine posture, snoring, and gastroesophageal reflux
cannot be dismissed. Directing therapy, perhaps in unique ways, may be
essential for the control of nocturnal asthma. Patients on inhaled
corticosteroid therapy or nonsteroidal anti-inflammatory agents often persist
in asthmatic disease expression at night. Long-acting bronchodilator therapy,
either by inhalation or with sustained-release tablets, is often added to
inhaled anti-inflammatory therapy for more complete 24-hour disease control.
Using existing therapies but employing chronotherapeutic strategies is likely
to improve the overall asthma management. By focusing on nocturnal asthma, we
may be able to improve our understanding of this disease and more effectively
control it over each 24-hour period.
Author(s):
Kujala
UM ; Sarna
S ; Kaprio
J ; Koskenvuo
M
Affiliation: Unit for Sports and Exercise Medicine, University of
Helsinki, Finland.
Title: Asthma and
other pulmonary diseases in former elite athletes. Source: Thorax (Thorax.) 1996 Mar; 51(3):
288-92
Abstract: BACKGROUND: The prevalence of asthma is rising and there are recent
reports of increasing asthma rates among top level skiers and runners in the
Nordic countries. METHODS: The lifetime occurrence of pulmonary diseases
(asthma, chronic bronchitis, emphysema) and current bronchitis symptoms was
compared in former elite male athletes (n = 1282) who represented Finland
between 1920 and 1965 at least once in international competitions and controls
(n = 777) who, at the age of 20, were classified as healthy and who responded
to a questionnaire in 1985. The presence of disease and symptoms was identified
from the questionnaire and, in the case of asthma, also from a nationwide
reimbursable medication register. The death certificates of the subjects of our
original cohort who died between 1936 and 1985 were also investigated to
determine the cause of death. RESULTS: The occurrence of the pulmonary diseases
was associated with age, smoking habits, occupational group, and a history of
exposure to chemicals. After adjusting for these variables, athletes who
participated in mixed sports (odds ratio (OR) 0.46, 95% confidence interval
(CI) 0.23 to 0.92) and power sports (OR 0.43, 95% CI 0.21 to 0.87) had lower
odds ratios for emphysema, and endurance sports athletes had a lower odds ratio
for the presence of at least one pulmonary disease (OR 0.53, 95% CI 0.28 to
0.98) when compared with controls. Athletes also tended to have fewer
reimbursable medications for asthma and fewer current symptoms for chronic
bronchitis. Between 1936 and 1985 two controls but none of the athletes died of
asthma. CONCLUSIONS: The lifetime occurrence of asthma or other pulmonary
diseases is not increased in former elite athletes, and exercise alone, even in
a cold environment, did not appear to increase the prevalence of asthma, at
least up to the mid 1980s.
Author(s):
Giesbrecht
GG ; Younes
M
Affiliation: Faculty of Physical Education and Recreation Studies,
University of Manitoba, Winnipeg.
Title: Exercise-
and cold-induced asthma. Source: Can J Appl Physiol (Canadian journal of applied physiology = Revue
canadienne de physiologie appliquee.) 1995 Sep; 20(3): 300-14
Abstract: Exercise- and cold-induced asthma are commonly recognized respiratory
disorders. The asthmatic response includes several factors contributing to
airway narrowing, and thus increased airway resistance. These include airway
smooth muscle contraction, mucus accumulation, and bronchial vascular
congestion as well as epithelial damage and vascular leakage. The etiology for
these disorders is nonantigenic. The primary stimulus is probably a combination
of airway cooling and drying (leading to hypertonicity of airway lining fluid).
Symptoms generally do not occur during the stimulus period (e.g., exercise)
itself. This protection may in part be due to increased catecholamine levels
during exercise. The early phase response, which occurs 5 to 15 min
poststimulus, may be mediated through a combination of (a) direct influences,
(b) vagal reflexes triggered by airway sensory receptors, or (c) responses to
mediator release. Spontaneous recovery occurs within 30 min to 2 hrs. There is
usually a refractory period of about 1 to 2 hrs during which responses to
further stimuli are attenuated. This may be due to depletion of histamine and
other mediators. As well, prostaglandin release (mediated via LTD4 which is
released during exercise) inhibits further airway narrowing. A late phase
response has been reported 4 to 10 hrs poststimulus in some patients. These
reactions are accompanied by a second release of histamine and other mediators
that cause inflammatory responses and epithelial damage. However, the exercise
dependence of this response is debated.
Author(s):
Becker
JM ; Rogers
J ; Rossini
G ; Mirchandani
H ; D'Alonzo
GE Jr
Affiliation: Section of Allergy, Asthma and Immunology, Department of
Pediatrics, St. Christopher's Hospital for Children, Drexel University College
of Medicine, Philadelphia, USA.
Title: Asthma
deaths during sports: report of a 7-year experience. Source: J Allergy Clin Immunol (The Journal of allergy and
clinical immunology.) 2004 Feb; 113(2): 264-7
Abstract: BACKGROUND: Asthma mortality and the mortality of athletes during sports have been described separately in detail in the medical literature. However, asthma has not been reported as a cause of death in competitive athletes. OBJECTIVE: The object of this study was to raise the awareness of physicians, coaches, trainers, and parents that children and adults can have fatal asthma exacerbations during and immediately after participating in sports. METHODS: The Temple Sports Asthma Research Center identified athletes from 1993 until 2000 who died during or after sporting activity by using the nationwide Burrell's Information Service. Once a possible asthma-related sports death was identified, the autopsy report was requested from the coroner or medical examiner, and an attempt was made to contact the family. Contact with the family was limited to information about the death, medical history, sports involvement, and any medication usage by the person who had died. Secondary sources, including news reports, were used to confirm whether the subject died of asthma during or immediately after a sporting activity. RESULTS: Two hundred sixty-three possible cases were identified. Sixty-one deaths met the criteria for study inclusion. White deaths outnumbered black deaths by 2 to 1. Deaths among male subjects predominated. Most subjects were younger than the age of 20 years, with the most prevalent age group being between 10 to 14 years old. Fifty-one percent (18 of 35) of the competitive athletes had their fatal event while participating in organized sport, 14 in a practice situation and 4 deaths during a game or meet setting. Basketball and track were the 2 most frequent activities performed at the time of the fatal event. CONCLUSION: The subjects who had fatal asthma exacerbations were usually white male subjects between the ages of 10 and 20 years. Mild intermittent or persistent asthma by history was commonly identified. Sudden fatal asthma exacerbations occur in both competitive and recreational athletes and can be precipitated by sporting activity.