Analysis of apoptosis and Bcl‐2 expression in polar forms of leprosy
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 p...
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| Veröffentlicht in: | FEMS immunology and medical microbiology 2010-12, Vol.60 (3), p.270-274 |
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| creator | Brito de Souza, Vânia Nieto Nogueira, Maria Esther Salles Belone, Andréa de Faria Fernandes Soares, Cleverson Teixeira |
| description | 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 |
| doi_str_mv | 10.1111/j.1574-695X.2010.00746.x |
| format | Article |
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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.</description><identifier>ISSN: 0928-8244</identifier><identifier>EISSN: 1574-695X</identifier><identifier>EISSN: 2049-632X</identifier><identifier>DOI: 10.1111/j.1574-695X.2010.00746.x</identifier><identifier>PMID: 20964723</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Apoptosis ; Bacillus ; Bcl-2 protein ; Bcl‐2 ; Cell death ; Cell survival ; Defense mechanisms ; Gene Expression ; Gene Expression Profiling ; Humans ; Immune status ; Immunohistochemistry ; In Situ Nick-End Labeling ; Infection ; Leprosy ; Leprosy, Lepromatous - pathology ; Leprosy, Tuberculoid - pathology ; Lesions ; Modulation ; Mycobacterium leprae ; Mycobacterium leprae - pathogenicity ; Pathogens ; Proto-Oncogene Proteins c-bcl-2 - biosynthesis ; Skin - pathology ; Skin diseases ; Skin lesions ; Survival ; TUNEL</subject><ispartof>FEMS immunology and medical microbiology, 2010-12, Vol.60 (3), p.270-274</ispartof><rights>2010 Federation of European Microbiological Societies. 2010</rights><rights>2010 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved</rights><rights>2010 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. 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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.</description><subject>Apoptosis</subject><subject>Bacillus</subject><subject>Bcl-2 protein</subject><subject>Bcl‐2</subject><subject>Cell death</subject><subject>Cell survival</subject><subject>Defense mechanisms</subject><subject>Gene Expression</subject><subject>Gene Expression Profiling</subject><subject>Humans</subject><subject>Immune status</subject><subject>Immunohistochemistry</subject><subject>In Situ Nick-End Labeling</subject><subject>Infection</subject><subject>Leprosy</subject><subject>Leprosy, Lepromatous - pathology</subject><subject>Leprosy, Tuberculoid - pathology</subject><subject>Lesions</subject><subject>Modulation</subject><subject>Mycobacterium leprae</subject><subject>Mycobacterium leprae - pathogenicity</subject><subject>Pathogens</subject><subject>Proto-Oncogene Proteins c-bcl-2 - biosynthesis</subject><subject>Skin - pathology</subject><subject>Skin diseases</subject><subject>Skin lesions</subject><subject>Survival</subject><subject>TUNEL</subject><issn>0928-8244</issn><issn>1574-695X</issn><issn>2049-632X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1O3DAUha2Kqgy0r1Aisegq0-vfxBIbQAwgUbFokbqz7MRGGWXi1CbqzI5H4Bl5EhxCWSAq8MZ_37nXPgehDMMcp_F9Oce8YLmQ_PecQDoFKJiYrz-g2fPFFpqBJGVeEsa20U6MSwBgEuAT2iYgBSsInaHFYafbTWxi5l2me9_f-HGjuzo7qtr72zuS2XUfbIyN77Kmy3rf6pA5H1aPktb2wcfNZ_TR6TbaL0_zLrpanPw6PssvLk_Pjw8v8oozLnJXGqgdlJpzSeqaYmcwEaYwusZEWulqwagwrKoKVpfGVhQzJitdcmq00UB30bepbur6Z7DxRq2aWNm21Z31Q1SlIIWkVJA3yUJQwhM6kvsvyKUfQrIlKkJBEI4F44kqJ6pK_43BOtWHZqXDRmFQYyhqqUbv1ei9GkNRj6GodZJ-fWowmJWtn4X_UkjAwQT8bVq7eXdhtTj_kRZJTie5H_r_iPPXXrU3qZz2Sl-HJqqrn4mggCXmQDl9ANufsww</recordid><startdate>201012</startdate><enddate>201012</enddate><creator>Brito de Souza, Vânia Nieto</creator><creator>Nogueira, Maria Esther Salles</creator><creator>Belone, Andréa de Faria Fernandes</creator><creator>Soares, Cleverson Teixeira</creator><general>Blackwell Publishing Ltd</general><general>Oxford University Press</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>7QL</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>201012</creationdate><title>Analysis of apoptosis and Bcl‐2 expression in polar forms of leprosy</title><author>Brito de Souza, Vânia Nieto ; 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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.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20964723</pmid><doi>10.1111/j.1574-695X.2010.00746.x</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | FEMS immunology and medical microbiology, 2010-12, Vol.60 (3), p.270-274 |
| issn | 0928-8244 1574-695X 2049-632X |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Oxford University Press Journals All Titles (1996-Current) |
| subjects | Apoptosis Bacillus Bcl-2 protein Bcl‐2 Cell death Cell survival Defense mechanisms Gene Expression Gene Expression Profiling Humans Immune status Immunohistochemistry In Situ Nick-End Labeling Infection Leprosy Leprosy, Lepromatous - pathology Leprosy, Tuberculoid - pathology Lesions Modulation Mycobacterium leprae Mycobacterium leprae - pathogenicity Pathogens Proto-Oncogene Proteins c-bcl-2 - biosynthesis Skin - pathology Skin diseases Skin lesions Survival TUNEL |
| title | Analysis of apoptosis and Bcl‐2 expression in polar forms of leprosy |
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