T lymphocyte subset profile and serum alpha-1-antitrypsin in pathogenesis of chronic obstructive pulmonary disease

doi:10.1111/j.1365-2249.2007.03429.x

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Wiley InterScience

Clinical & Experimental Immunology

Volume 149 Issue 3, Pages 463 - 469

Published Online: 12 Jun 2007

An Official Journal of the British Society for Immunology

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ORIGINAL ARTICLE

T lymphocyte subset profile and serum alpha-1-antitrypsin in pathogenesis of chronic obstructive pulmonary disease

J. Gupta,* D. Chattopadhaya, ^† D. P. Bhadoria, ^‡ M. A. Qadar Pasha,* V. K. Gupta, ^§ M. Kumar,* R. Dabur, ^¶ V. Yadav* and G. L. Sharma*

*Institute of Genomics and Integrative Biology, University Campus, Delhi, India, ^† Department of Microbiology, National Institute of Communicable Diseases, Delhi, India, ^‡ Department of Pulmonary Medicine, Guru Teg Bahadur Hospital and University, College of Medical Sciences, Shahdara, Delhi, India, ^§ Department of Biochemistry, Kurukshetra University, Kurukshetra, India, and ^¶ Department of Biochemistry, Regional Research Institute, Pune, India

Correspondence to G. L. Sharma, Institute of Genomics and Integrative Biology, Mall Road, University Campus, Delhi-110007, India.
E-mail: drglsharma@hotmail.com

KEYWORDS

alpha-1-antitrypsin • CD4⁺ T lymphocytes • CD8⁺ T lymphocytes • chronic obstructive pulmonary disease • inhibitory capacity • serum trypsin

Summary

Chronic obstructive pulmonary disease (COPD) is an inflammatory disorder characterized by the presence of non-fully reversible airflow limitation. The study was undertaken to investigate the involvement of alpha-1-antitrypsin (α₁AT) and T lymphocyte subsets in the pathogenesis of COPD. Blood samples of 50 subjects, including 25 healthy volunteers and 25 patients with COPD, were analysed. Serum trypsin inhibitory capacity (STIC) was determined by enzymatic assay. CD4⁺ and CD8⁺ T lymphocytes were enumerated in heparinized blood using a fluorescence activated cell sorter counter. The STIC in COPD patients was found to be decreased significantly than in controls (P < 0·01). In COPD patients with lower expression levels of α₁AT, a highly significant decrease in the number of CD4⁺ T lymphocytes (P < 0·0009) and CD4/CD8 ratio was observed compared with control subjects (P < 0·008). The mean ± standard error of CD8⁺ lymphocytes was found to be little different (only marginally decreased) in COPD patients compared to healthy controls; however, an alteration in the individual count of CD8⁺ lymphocytes cells was observed in COPD patients. Using linear regression analysis, a negative correlation was observed between STIC and CD4⁺ lymphocytes and CD8⁺ lymphocytes (r = −0·40, P < 0·04; r = −0·42, P < 0·03, respectively) in COPD patients. An alteration in α₁AT and T lymphocyte subsets in COPD patients suggested that interplay of these factors may be responsible for the progression of COPD.