Abstract
Hellcobacter pylori is the most common cause of gastroduodenal inflammation. However, the exact immune pathogenesis is not fully understood. To look for evidence of the immunological mechanism in H. pylori associated disease, we measured cytokine interleukin-2 (IL-2) and IL-4 levels produced by peripheral blood lymphocytes (PBL) and gastric biopsies in 20 subjects with or without H. pylori infection. H. pylori can stimulate IL-2 and IL-4 production from PBL in H. pylori negative as well as H. pylori positive individuals. The spontaneous IL-2 production by PBL and gastric biopsies was greater (p < 0.0025, <0.001)in H. pylori negative individuals than that in H. pylori infected patients. Increased IL-4 levels from PBL in H. pylori infected patients were found in the presence of H. pylori (p < 0.0025). An increased spontaneous production of IL-4 from gastric biopsies was also observed in H. pylori infected patients (p < 0.025). In conclusion, an enhanced type 2 cytokine production was observed in H. pylori infected patients, which may be responsible for H. pylori chronic infection.
Highlights
Helicobacter pylori are Gram-negative bacteria that live in the human stomach
IL-2 levels: H. pylori negative subjects had a significantl higher IL-2 level in supernatants from resting peripheral blood lymphocytes (PBL) compared with those having H. pylori infection
There was no significan difference between these two groups in IL-2 levels of supernatants from PBL, which were stimulated with PHA or H. pylori an increase in IL-2 production was found following
Summary
Helicobacter pylori are Gram-negative bacteria that live in the human stomach. H. pylori infection is recognized as one of the most common chronic infections in man. Pylori infection in gastroduodenal inflammation.- Colonization of the gastric epithelium by the bacterium results in an inflammatory reaction by both the humoral and cellular immune responses.[4] In spite of some established observations, the exact immune factors that contribute to pathogenetic mechanisms of the disease and that sustain the chronic colonization are not fully understood. TH1 cells produce interferon-gamma (IFN-,) and interleukin-2 (IL-2) which are associated with immunity or resistance to infection; whereas TH2 cells produce IL-4, IL-5, IL-6 and IL-10 cytokines which are associated with progression or persistence of infection. Cytokines produced by one type of TH cells can down-regulate the other type of TH cells. Enhanced TH2 reaction, which has an immunosuppressive role in human infection, has been found.5- To evaluate the respon-
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