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. 1999;8(4-5):237–243. doi: 10.1080/09629359990405

Lymphocytes apoptosis in patients with acute exacerbation of asthma.

A Hamzaoui 1, K Hamzaoui 1, H Salah 1, A Chabbou 1
PMCID: PMC1781801  PMID: 10704078

Abstract

Asthma is characterized by airway inflammation, which can be now assessed by the analysis of induced sputum. Ten patients with asthma were investigated during acute exacerbation for the quantification of apoptosis, for Bcl-2 and Fas expression, in induced sputum lymphocytes. They were compared to 12 patients with chronic obstructive pulmonary disease (COPD), and 10 healthy controls. Spontaneous apoptosis was determined by staining nuclei with propidium iodide, and analyzed with a FACScan. Bcl-2 was measured by Western blotting, and results were obtained by densitometric scanning, done by the gel proanalyser. The investigation of Fas was performed using the streptavidin-biotin preroxidase-complex method. Patients with asthma and patients with COPD exhibited a significant increase of cellularity, percentage of neutrophils, eosinophils and lymphocytes when compared to healthy controls. Apoptosis in induced sputum mononuclear cells was found decreased in patients with asthma compared to COPD patients and healthy controls. The quantification of apoptosis was measured after exposure to anti-cytokine antibodies. Anti-TNF-alpha antibody blocked the apoptosis in both patients groups and healthy controls, suggesting that TNF-alpha acted as an inducer of apoptosis. Anti-IL-10 blocked apoptosis completely exclusively in patients with asthma. Bcl-2 expression was found to be increased in induced sputum mononuclear cells from patients with asthma, compared to healthy controls and patients with COPD. Expression of Fas could be detected in patients with asthma, at a lower level than COPD patients and healthy controls. Distinct mechanisms of apoptosis were found in patients with asthma and patients with COPD, characterized by different levels of Bcl-2 and Fas expression. Induction of apoptosis should be a beneficial process in allergic inflammation traduced in induced sputum mononuclear cells. The apoptosis process is assumed by two different mechanisms in asthma and COPD. Our findings indicated that in asthmatic patients, activated lymphocytes accumulate in the bronchi; because of their prolonged survival that maintains inflammation.

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Selected References

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  1. Barnes P. F., Chatterjee D., Brennan P. J., Rea T. H., Modlin R. L. Tumor necrosis factor production in patients with leprosy. Infect Immun. 1992 Apr;60(4):1441–1446. doi: 10.1128/iai.60.4.1441-1446.1992. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Fahy J. V., Liu J., Wong H., Boushey H. A. Cellular and biochemical analysis of induced sputum from asthmatic and from healthy subjects. Am Rev Respir Dis. 1993 May;147(5):1126–1131. doi: 10.1164/ajrccm/147.5.1126. [DOI] [PubMed] [Google Scholar]
  3. Grootendorst D. C., van den Bos J. W., Romeijn J. J., Veselic-Charvat M., Duiverman E. J., Vrijlandt E. J., Sterk P. J., Roldaan A. C. Induced sputum in adolescents with severe stable asthma. Safety and the relationship of cell counts and eosinophil cationic protein to clinical severity. Eur Respir J. 1999 Mar;13(3):647–653. doi: 10.1183/09031936.99.13364799. [DOI] [PubMed] [Google Scholar]
  4. Hamzaoui K., Hamzaoui A., Zakraoui L., Chabbou A. Expression of Bcl-2 in inflammatory sites from patients with active Behçet's disease. Mediators Inflamm. 1999;8(2):101–106. doi: 10.1080/09629359990595. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Hargreave F. E., Popov T., Kidney J., Dolovich J. Sputum measurements to assess airway inflammation in asthma. Allergy. 1993;48(17 Suppl):81–86. doi: 10.1111/j.1398-9995.1993.tb04705.x. [DOI] [PubMed] [Google Scholar]
  6. Hebestreit H., Yousefi S., Balatti I., Weber M., Crameri R., Simon D., Hartung K., Schapowal A., Blaser K., Simon H. U. Expression and function of the Fas receptor on human blood and tissue eosinophils. Eur J Immunol. 1996 Aug;26(8):1775–1780. doi: 10.1002/eji.1830260817. [DOI] [PubMed] [Google Scholar]
  7. Matsumoto K., Schleimer R. P., Saito H., Iikura Y., Bochner B. S. Induction of apoptosis in human eosinophils by anti-Fas antibody treatment in vitro. Blood. 1995 Aug 15;86(4):1437–1443. [PubMed] [Google Scholar]
  8. Ohta K., Yamashita N. Apoptosis of eosinophils and lymphocytes in allergic inflammation. J Allergy Clin Immunol. 1999 Jul;104(1):14–21. doi: 10.1016/s0091-6749(99)70107-7. [DOI] [PubMed] [Google Scholar]
  9. Rowbottom A. W., Lepper M. A., Garland R. J., Cox C. V., Corley E. G. Interleukin-10-induced CD8 cell proliferation. Immunology. 1999 Sep;98(1):80–89. doi: 10.1046/j.1365-2567.1999.00828.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Schulze-Osthoff K. The Fas/APO-1 receptor and its deadly ligand. Trends Cell Biol. 1994 Dec;4(12):421–426. doi: 10.1016/0962-8924(94)90102-3. [DOI] [PubMed] [Google Scholar]
  11. Taga K., Cherney B., Tosato G. IL-10 inhibits apoptotic cell death in human T cells starved of IL-2. Int Immunol. 1993 Dec;5(12):1599–1608. doi: 10.1093/intimm/5.12.1599. [DOI] [PubMed] [Google Scholar]
  12. Zheng L., Fisher G., Miller R. E., Peschon J., Lynch D. H., Lenardo M. J. Induction of apoptosis in mature T cells by tumour necrosis factor. Nature. 1995 Sep 28;377(6547):348–351. doi: 10.1038/377348a0. [DOI] [PubMed] [Google Scholar]

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