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Analysis of apoptosis and Bcl-2 expression in polar forms of leprosy.
MedLine Citation:
PMID:  20964723     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
Apoptosis eliminates pathogen-infected cells. Its modulation can influence the course of infections, permitting the survival of intracellular pathogens. In leprosy, which presents several clinical manifestations related to bacillary burden and host immune status, the mechanisms responsible for the persistence of the bacillus are unknown. Few studies have focused on apoptosis over the disease spectrum and as a defense mechanism against Mycobacterium leprae. We evaluated apoptosis using terminal transferase dUTP nick end labeling and the expression of Bcl-2 by immunohistochemistry in skin lesions from 11 tuberculoid and 15 lepromatous leprosy patients. Each specimen was evaluated by determining the number of positive cells in 10 fields at × 400 magnification. We observed a higher number of apoptotic cells in tuberculoid lesions in comparison with lepromatous leprosy (42.5 cells per 10 fields vs. 11.5 cells per 10 fields, P<0.0001). Expression of Bcl-2, conversely, was larger in lepromatous than in tuberculoid samples (172.0 cells per 10 fields vs. 17.7 cells per 10 fields, P<0.0001). These observations suggest modulation of apoptosis in leprosy, primarily in lepromatous patients, for which the decrease in cell death could support M. leprae survival and contribute to the success of infection. Conversely, in tuberculoid patients, apoptosis could contribute to reducing propagation of the bacillus.
Authors:
Vânia Nieto Brito de Souza; Maria Esther Salles Nogueira; Andréa de Faria Fernandes Belone; Cleverson Teixeira Soares
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-10-21
Journal Detail:
Title:  FEMS immunology and medical microbiology     Volume:  60     ISSN:  1574-695X     ISO Abbreviation:  FEMS Immunol. Med. Microbiol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-09     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9315554     Medline TA:  FEMS Immunol Med Microbiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  270-4     Citation Subset:  IM    
Copyright Information:
© 2010 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved.
Affiliation:
Equipe Técnica de Imunologia, Instituto Lauro de Souza Lima, Bauru, São Paulo, Brazil. vbrito@ilsl.br
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