IMPAIRED PHAGOCYTE OXIDATIVE CAPACITY IN PATIENTS WITH HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION

Citation
Dl. Pitrak et al., IMPAIRED PHAGOCYTE OXIDATIVE CAPACITY IN PATIENTS WITH HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION, The Journal of laboratory and clinical medicine, 132(4), 1998, pp. 284-293
Citations number
36
Categorie Soggetti
Medicine, General & Internal","Medicine, Research & Experimental","Medical Laboratory Technology
ISSN journal
00222143
Volume
132
Issue
4
Year of publication
1998
Pages
284 - 293
Database
ISI
SICI code
0022-2143(1998)132:4<284:IPOCIP>2.0.ZU;2-Z
Abstract
Bacterial infections that may be related to impaired phagocyte functio n often develop in patients infected with human immunodeficiency virus (HIV). We examined the oxidative capacity of circulating phagocytes i n 78 HIV+ patients and 31 control subjects by measuring chemiluminesce nce with a whole blood assay. Phagocytes were stimulated with zymosan opsonized with human complement (hC-OPZ) or immunoglobulin (hI-OPZ) wi th or without exogenous primers. Patients with CD4(+) < 500/mu L showe d reduced whole blood chemiluminescence at maximal opsonin receptor (M OR) activity after priming in response to hC-OPZ relative to control s ubjects, and the difference was significant for patients with CD4(+) < 100/mu L. Patients had lower absolute phagocyte counts; however, the chemiluminescence activity calculated per phagocyte count was signific antly depressed in advanced HIV infection, indicating the impairment o f phagocytic cell function and a reduction in number. Data were simila r when hI-OPZ was used as a stimulus. The chemiluminescence of unprime d phagocytes at circulating opsonin receptor (COR) activity relative t o maximally primed phagocytes (COR/MOR ratio) was significantly higher for HIV+ patients as compared with control subjects and indicates a d efect in phagocyte priming. Alternatively the phagocytes do not increa se chemiluminescence with priming because they have already been prime d or activated in vivo. In late-stage disease, decreased opsonin recep tor-dependent respiratory burst activity contributes to the risk of se condary bacterial infections.