Abstract: Slide Presentations |


Nazima Nisar, PhD*; Randeep Guleria, MD; Sanjay Kumar, MSc; Tirlok C. Chawla, PhD; Niranjan Nayak, MD; Arvind K. Singh, MBBS; Nihar R. Biswas, MD
Author and Funding Information

All India Institute of Medical Sciences, New Delhi, India

Chest. 2006;130(4_MeetingAbstracts):96S. doi:10.1378/chest.130.4_MeetingAbstracts.96S-b
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PURPOSE:Mycoplasma pneumoniae ( M. pneumoniae), best known for causing tracheobronchitis and atypical pneumonia in human, has recently been associated with asthma. The pathophysiological mechanisms by which the pathogen contributes to the development of asthma are not fully understood. Recently it has been shown that interleukins (IL-4, IL-5, IL-9 and IL-13) are central biological triggers of asthma. It has been hypothesized that M. pneumoniae infection may cause airway inflammation by inducing Th-2 immune response with increased airway expression of various interleukins.The purpose of the present study is to see the seropositivity of M. pneumoniae in asthmatics and correlate the levels of Interleukin-5 (IL-5) with M. pneumoniae positive /negative subjects.

METHODS: One hundred and forty six stable asthma patients were enrolled. Diagnosis of asthma was confirmed on clinical basis and lung functions with reversibility. Serum samples collected from these patients were subjected to serological examination for IgM and IgG antibodies to M. pneumoniae using gelatin particle agglutination assay and enzyme linked immunosorbent assay respectively. Subsequently, serum samples were randomly selected from both M. pneumoniae positive (n-26) and M. pneumoniae negative patients (n-26) to estimate the concentration of IL-5 using Immunotech- IL-5 enzyme immunoassay.

RESULTS: Seropositivity to M. pneumoniae specific IgM antibodies in asthmatics was found to be 25% (37/146) whereas 45% ( 36/80) were seropositive for IgG antibodies. With regards to cytokine expression, there was no difference in baseline expression of IL-5 between M. pneumonaie positive and M. pneumoniae negative subjects.

CONCLUSION: In the present study, almost half of stable asthmatics studied showed an evidence of M. pneumoniae infection. However, an association between M. pneumoniae infection and IL-5 could not be found. Further studies are warranted to assess the involvement of other inflammatory markers in asthmatics with M. pneumoniae infection.

CLINICAL IMPLICATIONS: The present study suggests that M. pneumoniae may play an important role in the etiopathogenesis of asthma. Treatment strategies targeting M. pneumoniae in addition to standard therapy may help in a subset of patients having M. pneumoniae infection for a better control of asthma.

DISCLOSURE: Nazima Nisar, None.

Monday, October 23, 2006

2:30 PM - 4:00 PM




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