T-cell immunity in human chronic toxoplasmosis

Toxoplasmosis is a disease affecting 500 million people worldwide. The seroprevalence varies [from 5% to 90%], depending on geographical location, age, habit of eating raw meat or unwashed fruit and vegetables, and general level of hygiene. The incidence of infections is higher in warmer and humid climate and increases with age. The disease can be congenital or acquired. Cell response [TNF-alpha and IFN-gamma secreted by Th1 cells] and humoral response [IL-4, and IL-10 secreted by Th2 cells] were evaluated. This study assessed the effect of T. gondii on chosen indices of the immune response. The study involved 45 women infected with T. gondii [aged 18-42 years] proven have a chronic toxoplasmosis [IgG positive and IgM negative]. The control group consisted of 25 healthy women [aged 18-45 years] [IgG and IgM negative]. The results showed that patients infected with T. gondii had increased production of theTh-1 cytokines involved TNF-alpha and IFN-gamma that responsible for the cellular response compared to controls. Also, increased production of Th2 cytokines involved IL-4 and IL-10 that responsible for humoral response compared to controls

Decreased Helicobacter pylori-associated gastric epithelial proliferation by concurrent Schistosomal infection

Helicobacter pylori [H. pylori] injection is associated with increased gastric epithelial proliferation, the enhanced epithelial proliferation is important in developing gastric carcinoma. Some developing countries with a high prevalence of H. pylori infection have high gastric cancer rates, whereas in others, these rates are low. The progression of helicobacter-induced gastritis and gastric atrophy mediated by T-helper cell, type 1 [Th1] response may be modulated by concurrent parasitic infection. Pathogenic helminths of the genus Schistosoma cause T-helper cell, type 2 [Th2] response to parasite eggs. The Th2 response is usually associated with down regulation of Th1 cytokine synthesis. The aim of the present study was to assess whether concurrent Schistosoma mansoni infection with H. pylori has an effect on gastric mucosal injury in view of cell proliferation, apoptosis, pathological changes, nitric oxide and oxyradicals status. Between April 2001 and March 2002, 73 patients [13 child and 60 adults] were subjected to upper gastrointestinal endoscopy for dyspepsia and liver cirrhosis in the National Liver Institute, Menoufiya University. Four biopsy specimens were taken, two from the greater curvature of the antrum and two from the upper body of the stomach, biopsies were obtained from any lesion as well as from apparently healthy mucosa. One snap from each site was preserved in RNA later solution, then kept at -80°C till utilized for estimation of DNA-flow cytometric assay, reduced glutathion [GSH], catalase [CAT], superoxide dismutase [SOD], Nitric oxide [NO], and lipid peroxidation product- malondialdehyde [MDA]-. Diagnosis of bilharziasis was done by stool analysis, or by sigmoidoscopy and rectal snip. OF the 73 patients, 60 patients were cirrhotic [20 Child A, 34 B, 6 C], 48 were H. pylori-positive and 25 H. pylori negative. The mean age in H. pylori positive patients [46.31 +/- 10.7 years] was significantly less than in H. pylori - negative patients [52.8 +/- 7.2 years]. Infection with H. pylori alone correlated with increased DNA s-phase, proliferation activity and apoptosis [sub-G phase] [p 0.04, 0.03 and 0.04] respectively. Concurrent infection with schistosomiasis occurred in 34 patients and it significantly suppressed DNA 5-phase [P=0.001], proliferation activity [p<0.004], and apoptosis [sub-G phase], [p>0.05]. On contrast, concurrent infection had an adverse effect on liver cirrhosis with increased incidence of upper gastrointestinal bleeding. Schistosomal concurrent infection with H. pylori is associated with higher incidence of superficial gastritis, and may complicate liver cirrhosis with increased upper gastrointestinal bleeding. On the other hand, concurrent schistosomal infection may have a protective effect against the possible progression of H. pylori induced gastritis towards gastric carcinoma, by modulating the cytokine profile of the gastric mucosa with suppression of the proliferation activity. A detailed study of the cytokine expression in similar cases is recommended for unraveling the mystery of this phenomenon