Bronchial asthma is a chronic inflammatory disorder of
the airway in which many cells play a role, in
particular, mast cells, eosinophils and T- lymphocytes.
It is characterized by airway hyperresponsiveness with
recurrent episodes of wheezing, breathlessness.
Chest tightness and cough, particularly at night and or
in the early morning. These symptoms are usually
associated with widespread, but variable. Airflow
limitation that is at least partly reversible, either
spontaneously or with treatment (1).
Asthma is a worldwide problem and occurs in all races,
but its prevalence varies from less than 1% to as high
as 305 of population in different countries.
In addition to the inflammatory basis of asthma, it is
well established that asthma is a complex genetic
disease that can not be explained by a single gene and
results from interaction between genetic and
environmental factors e.g. allergens. Viral infections,
occupational stimuli, fogs, fumes, exercise, drug,
gastroesophageal reflux and emotional factors (1).
Clamydia are obligate intracellular gram negative
eubacteria. Chlamydia pneumonia strain TWAR was named in
1989 as a new member of the Chlamydia family C.
trachomatis, C. psittaci and C. pecorum .
The strain was called TWAR, an acronym reflecting the
history of the first two isolates, Taiwan, and acute
respiratory (2) .
Chlamydia pneumonia is a common respiratory pathogen and
is transmitted from human to human with no intervening
avian or mammalian host, and is responsible for 10% of
community- acquired pneumonia and 5% of bronchitis
The unique Chlamydia intracellular life cycle and the
propensity for human Chlamydia infection to become
persistent results in immunopathologic, and inflammatory
damage in target organ (2).
It is recently that reported that Chlamydia pneumonia is
associated with bronchial with bronchial asthma,
atherosclerosis, multiple sclerosis and lung cancer and
C. pneumonia may trigger acute exacerbation of adult
Aim of The Work:
The aim of this study is to assess the prevalence of
Chlamydia pneumonia infection in adult patients with
bronchial asthma and attempt to find out if there is a
possible casual association between Chlamydia pneumonia
Subjects and Methods:
The present study was conducted on three groups:
Group1: 85 patients with acute asthma.
Group2: 78 patients with chronic stable asthma.
Group3: 65 control subjects.
All groups were matched for age, sex and were never
Patients with acute asthma were subjected to the
Complete history and clinical
Peak expiratory flow (PEF) rate
to assess reversibility of airway obstruction, using
mini- Wright peak flowmeter.
Serum samples from all subjects were tasted for
Chlamydia pneumonia – specific antibodies (IgG) using
enzyme immunoassay (EIA) test (5). Acute
infection with Chlamydia pneumonia was defined by titres
of IgG > 512 and previous infection by IgG 16- 256.
Table (1): Age distribution
Chronic stable asthma
Table (2): sex distribution
Table (3): serologic evidence of Chlamydia pneumonia infection in
patients with acute asthma:
Acute infection(IgG> 512 )
Previous infection (IgG 16- 256)
14 / 85
31 / 85
Table (4): serologic evidence of previous infection with Chlamydia
pneumonia in patients with chronic stable asthma &
Chronic stable asthma
36 / 78
2 / 65
pneumonia has been recently linked to asthma in the way
that infection may precede asthma onset or make asthma
control more difficult (6).
The present study showed that IgG titre suggesting acute
Chlamydia pneumonia infection (IgG titre> 512) occurred
in 14 (16.5) patients with acute asthma (table 3). This
result is compatible with that reported by Miyashita et
Thus, Chlamydia pneumonia may trigger acute exacerbation
of bronchial asthma, and this may be explained by the
ability of Chlamydia pneumonia to elicit T- helper cell
(TH2 ) response and promote airway inflammation and
development of atopic inflammatory response(6).
On the other hand, cellular components of Chlamydia
pneumonia are a potent stimulus of cytokine production
as interleukin-1, interleukin-6, monocyte
chemoattractant protein-1 (MCP-1) and macrophage
inflammatory protein-1 (MIP-1). This mechanism may have
a role in inflammatory aspect of asthma (7).
IgG titre suggesting previous Chlamydia pneumonia
infection (IgG 16-256) was found in 31 (36.5 %)
patients with acute asthma (table 3), 36(46.2%)
patients with chronic stable asthma and 2 (3.1 %)
controls (table 4).
The prevalence of Chlamydia pneumonia seroreactivity is
significancy higher in both acute asthma and chronic
stable asthma than in controls (p<0.001). These results
are in agreement with those found by Cunningham et al
The host cells of Chlamydia pneumonia are respiratory
columnar epithelial cells and smooth muscle cells and
the persistence of Chlamydia pneumonia seroreactivity in
patients with chronic asthma lead to increased
production of IL-6 and basic fibroblast growth factor (bFGF).
This cytokine response may contribute to structural
remodeling in the airway in chronic asthma (9).
Our data suggest that Chlamydia pneumonia infection may
trigger acute exacerbation of adult asthma. The high
prevalence of persistent Chlamydia pneumonia
seroreactivity in chronic stable asthma raises its
possible role in the pathogenesis of bronchial asthma,
but this remains to be established.
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