Open AccessColonization of gerbils with H elicobacter pylori O ‐chain‐deficient mutant SS 1 HP 0826:: K an results in gastritis and is associated with de novo synthesis of extended homopolymers
Author(s) -
Chandan Vandana,
Jeremy Anthony H.T.,
Dixon Michael F.,
Altman Eleonora,
Crabtree Jean E.
Publication year - 2013
Publication title -
pathogens and disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.983
H-Index - 105
ISSN - 2049-632X
DOI - 10.1111/2049-632x.12021
Subject(s) - helicobacter pylori , gastritis , biology , microbiology and biotechnology , gerbil , mutant , metaplasia , intestinal metaplasia , atrophy , pathology , gene , medicine , biochemistry , genetics , ischemia
The O ‐chain polysaccharide of H elicobacter pylori is important for colonization and generation of chronic gastritis in mice. There are marked host differences in the development of H . pylori ‐induced gastric pathology in mice and gerbils. To investigate the role of the O ‐chain polysaccharide of H . pylori in colonization and gastritis in M ongolian gerbils, inoculation by oral gavage with H . pylori strain SS 1 and its corresponding O ‐chain polysaccharide‐deficient mutant SS 1 HP 0826:: K an was undertaken. Infection with both strains resulted in corpus atrophy, loss of parietal cells, and extensive mucous metaplasia at both 18 and 30 weeks postinfection. Contrary to previous results in splenocyte recipient severe combined immunodeficiency ( SCID ) mice, no difference was found in the grade of chronic gastritis, polymorphonuclear cell infiltration, atrophy, and mucous metaplasia in gerbils infected with the wild‐type SS 1 strain or SS 1 HP 0826:: K an strain. Examination of the effects of gerbil passage on LPS profiles of output SS 1 HP 0826:: K an isolates by SDS ‐ PAGE , sugar, and methylation analyses revealed significant differences in LPS profiles of SS 1 HP 0826:: K an cells recovered from infected gerbils as compared to input bacteria. Specifically, the presence of a novel homopolymer of d ‐galactan, as well as an extended polymer of d ‐riban, was detected. These data provide evidence for the role of H . pylori LPS in bacterial adaption to promote colonization and pathology.