Chlamydia Pneumonia and Bronchial Asthma

Abstract:

 OJECTIVES: To assess the prevalence of Chlamydia ( C ) pneumonia infection and its possible association with adult asthma.

METHODS: 85 adult patients with acute asthma, 87 patients with chronic stable asthma and 65 control subjects matched for age, sex and smoking status were tested for C. pneumonia specific antibodies (IgG) by enzyme immunoassay (EIA). Acute infection was defined by titers of IgG> 512 and previous infection by IgG 16-256.

Results: Serologic evidence of acute infection with C.

Pneumonia was present in 14 (16.5%) of patients with acute asthma and serologic evidence of previous infection with C. pneumonia was found in 36 (46.2%) of patients with chronic stable asthma and 2 (3.1%) of controls. Significantly higher in acute asthma and chronic stable asthma than in controls (p< 0.001).

Conclusions: our data suggest that C. pneumonia infection may trigger acute exacerbation of adult asthma. The high prevalence of persistent C. pneumonia seroreactivity in chronic stable asthma raises its possible role in the pathogenesis of bronchial asthma but this remains to be established.  
 

Introduction:

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 ⁽³⁾.

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 asthma⁽⁴⁾.

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 and asthma.

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 smokers.

Patients with acute asthma were subjected to the following:

-         Complete history and clinical examination.

-         Chest radiograph.

-         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.

Results

 Table (1): Age distribution

Table (2): sex distribution

Table (3): serologic evidence of Chlamydia pneumonia infection in patients with acute asthma:

 Table (4): serologic evidence of previous infection with Chlamydia pneumonia in patients with chronic stable asthma & controls:

 Discussion:

 Chlamydia 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 al ⁽⁴⁾.

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 ⁽⁸⁾ .

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⁾.

Conclusion:

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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