Immune Response
Authors: H Pylori, Cytokines Ernst, H Haberle, Lipopolysaccharide Crabtree, B Ye, C Barrera, H Gunasena, S Crowe, V Reyes, " Rembacken, U Lindley, A Moran
Journal: Gut (1995)

The gastrointestinal epithelium is believed to induce tolerance in Dept.Microbiology, Univerity College, Galway, Eire epithelial T cells under normal conditions.During inflammation, Purpose.IL-8 secretion is induced in gastric epithelial cell epithelial cells may become immunogenic and have the potential to lines by H. pylori (Hp) in a strain-specific manner.The activate CD4+ T cells.The induction of anergy or reactivity may be response of gastric epithelial cells to lipopolysaccharide controlled by the differential expression of adhesion molecules (LPS) of gastrointestinal flora is relevant to both Hp-induced necessary for T cell activation.As there is a marked infiltration of chronic gastritis and bacterial overgrowth in the achlorhy- the gastric epithelium with activated CD4 T cells during infection effects of LPS from different bacteria on IL-B secretion from with H. pylor;, we have studied the effect of cytokines induced gastric and colonic cell lines.during infection with H. pylori, as well as H. pylo~a lone, on the Methods.Gastric (AGS, Kato 3, ST42) and colonic (HT29c expression of accessory molecules by the gastric epithelium.The SW480) epithelial cell lines (5 x 1 0) were stimulated with human gastric epithelial cell line, Kato IlIl, expresses low levels of 1 Ong/mI -50 pg/ml of LPS from Hp, Escherichia coli (Ec)class 11 MHC molecules as well as ICAM-1 and LFA 3 as measured by and Salmonella typhimurium (St) in the presence or absence flow cytometry.Staining with an antibody to B7.1 was negative, of fetal calf serum.Secreted IL-8 over 24 hours was however, CTLA4-1g does bind which implies that Kato 11 may express assayed by ELISA.B7.2 or B7.3.Stimulation of the cells with 100 U/mI of IFN-y for 48Results.In all 3 gastric cell lines no IL-8 secretion occurred hr increased the expression of MHC molecules and ICAM-1 but had in response to St and Ec LPS.In 2 gastric cells (AGS and no effect on LFA-3 and the various forms of B7.Cross-linking of the Kato-3), in the presence of serum, low level secretion of IL- MHC class 11 molecules with monoclonal antibodies or microbial 8 above controls was observed with high concs. of Hp LPS MHcasgs moincreased with CTLA4-lg anti-B7ial (AGS: 5Opg LPS, 0.45 ng/ml IL-8; Kato-3: 50ug/ml LPS, superantigens icesdtesannwihCL4gbunoati371.01 ng/ml IL-8, 2.5 pg/mI LPS, 0.83ng/ml).The gastric cell mAb, again, suggesting that the gastric epithelium expresses more line ST42 was more responsive to Hp LPS (1 Opg/mI LPS, B7.2 or B7.3 than B7.1 and may play a role in the activation of 1.9 ng/ml IL-8) showing a dose-dependent increase in IL-8 memory T cells that can be found in the epithelium of individuals secretion with LPS conc.> 1pg/ml.In the intestinal cell infected with H. pylori.The addition of H. pylo~a lone had little lines maximal IL-8 secretion was induced by Ec LPS.HT29 effect on the expression of surface molecules.Thus, cytokines and SW480 were poorly responsive to Hp LPS, the concs.induced during H. pylo~i nfection may increase the expression of required to induce IL-8 being 1000-fold higher than with Ec class 11 MHC molecules followed by B7.2 and/or B7.3.This LPS.IL-8 induction by LPS was serum dependent, secretion combination of MHC and accessory molecules could facilitate the of IL-8 being reduced in serum-free cultures.persistent activation of memory T cells within the epithelium and Conclusions.In gastric cell line ST42 Hp LPS shows a contribute to gastric inflammation and the B cell proliferation preferential ability to induce IL-8 secretion relative to the observed in the tissue from these patients.Supported in part by NIH LPS of other organisms.Reciprocal results were observed