Effects of polysaccharide isolated from Streptococcus thermophilus CRL1190 on human gastric epithelial cells.

EPS1190 was isolated from skim milk fermented with Stretococcus thermophilus CRL1190. The polysaccharide consisted of 33% glucose and 66% galactose with 1,4- and 1,4,6-galactose residues as main building blocks beside a high amount of 1,4-linked glucose. The polymer was characterized additionally concerning viscosity and zeta potential. EPS1190 stimulated cellular vitality and proliferation of human stomach AGS cells and human buccal KB cells significantly. EPS1190 stimulated phagocytosis rate of murine macrophages RAW264.7 significantly. NO-release or anti-inflammatory effects by inhibition of LPS-induced NO release were not observed. Confocal laser scanning microscopy revealed that EPS1190 is partially internalized into AGS cells via endosomes. The bioadhesive absorption of FITC-labeled EPS1190 into the mucus layer on the apical side of the epithelium using histological tissue sections from human stomach was observed. Specific interaction of EPS1190 with mucin can be excluded as shown by microviscosimetry studies. EPS1190 increased the adhesion of H. pylori to AGS cells, which resulted in increased secretion of proinflammatory cytokines TNFa, IL-6 and IL-8. Summarizing, EPS1190 seems to stimulate epithelial cell regeneration and immunological innate defense mechanisms, which again can rationalized the use of this polysaccharide as cytoprotective compound in probiotioc preparations.

Prevalence and specificity of antigastric autoantibodies in adolescents infected with Helicobacter pylori.

OBJECTIVES: Antigastric autoantibodies (AGA) can be detected in as many as 50% of adults infected with Helicobacter pylori. We investigated H pylori -associated antigastric autoimmunity in children and adolescents. STUDY DESIGN: Patients with dyspepsia (n = 78; mean age 10.9 years, range 2-21 years, SE 0.46 years) underwent gastroscopy. H pylori infection was determined by serologic and histologic features and breath tests. AGA were detected by immunohistochemistry and were characterized by immunoprecipitation with the gastric hydrogen ion, potassium ion, adenosine triphosphatase (H(+),K(+)-ATPase). In absorption assays, antibodies against H pylori were removed to determine the role of molecular mimicry. RESULTS: AGA were detected in 9 (18%) of the 51 infected patients and in 1 (4 %) of the 27 noninfected patients (P =.08; nonsignificant) and could not be absorbed to H pylori. Children with AGA were significantly older (P =.01). AGA in H pylori gastritis reacted against the gastric H(+),K(+)-ATPase in 3 (33%) of the 9 patients. CONCLUSIONS: The age of the patient or the duration of gastritis seem to be relevant factors for the formation of antigastric autoimmunity. The gastric H(+),K(+)-ATPase represents an autoantigen as early as childhood. No evidence for a role of molecular mimicry between H pylori and the host at this young age could be found.