الفهرس 
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Abstract
Infectious agents, from viruses to parasites, can either delay or induce apoptosis of different types of host cells. This study was carried out to investigate the expression of the apoptosis related proteins Fas (CD95), Bcl2, and NF B in peripheral blood mononuclear cells (PBMCs) from patients with different infectious diseases and to evaluate the contribution of peripheral blood T cell apoptosis to the development and maintenance of the different clinical forms of these diseases. METHODS: Peripheral blood from 79 patients with different stages of chronic hepatitis C (HCV), chronic hepatitis B (HBV), schistosomiasis, toxoplasmosis, and chronic mucocutaneous candidiasis, as well as 10 healthy control subjects, was investigated for morphological detection of apoptotic PBMCs, in addition to the expression of Fas (CD95), Bcl2, and NF B. These parameters were compared between different patient groups as well as with normal uninfected control subjects. RESULTS: Morphological detection of apoptotic cells demonstrated significantly increased levels of PBMC apoptosis in all the studied groups when compared with controls (p0.001), which was associated with significantly increased expression of Fas in patients with chronic hepatitis, this being more profound in decompensated than in compensated patients (64.6% vs. 41.4% for HCV; 80.5% vs. 52.4% for HBV; while NF B expression was significantly decreased (55.5% vs. 33.3% for HCV; 50% vs. 30% for HBV;. Only intestinal, but not hepatosplenic, schistosomiasis patients showed increased Fas expression (46.5%;) in addition to decreased NF B expression (44.4%) while patients with toxoplasmosis and chronic mucocutaneous candidiasis also showed increased expression of Fas (17.73% and 35.7%, respectively; as well as decreased NF B expression in 50% of patients in both groups. Bcl2 expression was found to be comparable to controls in all studied groups (p>0.05). CONCLUSION: Apoptosis occurs in a wide variety of infectious diseases, and may be related to disease progression and severity, especially in chronic hepatitis. This was mainly as a result of increased surface expression of proapoptotic Fas, with decreased expression of antiapoptotic NF B and lack of expression of antiapoptotic Bcl2.