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Altered Expression of CD88 and Associated Impairment of Complement 5a–Induced Neutrophil Responses in Human Immunodeficiency Virus Type 1–Infected Patients with and without Pulmonary Tuberculosis
Author(s) -
Stephen MeddowsTaylor,
Stella Pendle,
Caroline T. Tiemessen
Publication year - 2001
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/318532
Subject(s) - coinfection , immunology , tuberculosis , mycobacterium tuberculosis , flow cytometry , degranulation , complement receptor , complement system , virus , virology , medicine , biology , antibody , receptor , pathology
The effect of infection with human immunodeficiency virus type 1 (HIV patient group), infection with Mycobacterium tuberculosis (TB patient group), and coinfection with both of these organisms (HIV/TB patient group) on the expression of CD88 on polymorphonuclear leukocytes (PMNL) was determined by using a receptor-specific monoclonal antibody and flow cytometry. A significant reduction in the fluorescence intensity of CD88 on PMNL was observed in the HIV and HIV/TB groups, compared with both the healthy donor (HD) and TB groups. Furthermore, when degranulation of PMNL was induced by ligation of CD88 by complement 5a (C5a), a large proportion of patients in the HIV and the HIV/TB groups was found to have reciprocal degranulation responses. Patients in the 2 HIV groups also were found to have significantly reduced C5a-induced chemotactic responses and significantly elevated peripheral levels of C5a des Arg, compared with the HD and TB groups. These differences may contribute to the increased susceptibility of HIV-1-infected individuals to secondary microbial infections.

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