Schistosoma haematobium-induced urinary tract morbidity correlates with increased tumor necrosis factor-alpha and diminished interleukin-10 production

This study examined the hypothesis that the nature of the host cellular immune response to schistosome ova is a risk factor for urinary tract morbidity in areas in which Schistosoma haematobium is endemic. S. haematobium–infected children and adolescents with bladder pa-thology assessed by ultrasonography had 54-fold greater tumor necrosis factor (TNF)–a pro-duction and a 120-fold greater ratio of TNF-a to interleukin (IL)–10 release by peripheral blood mononuclear cells in response to egg antigens, in comparison with control children and adolescents matched by age, sex, and infection severity. Mycobacterial antigens also stimulated 7-fold more TNF-a among subjects with bladder morbidity than in control subjects, which suggests an innate predisposition to enhanced TNF-a production. Levels of egg antigen– induced IL-4 and-5 and interferon-g were equivalent in subjects with and without bladder pathology. Thus, children and adolescents predisposed to increased TNF-a production to S. haematobium infection are more likely to develop an exaggerated granulomatous response to ova trapped in the bladder wall, with associated urinary tract pathology. Schistosomiasis is caused by infection with the parasitic trematode of the genus Schistosoma. Adult Schistosoma hae