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Helicobacter pylori outer membrane proteins on gastric mucosal interleukin 6 and 11 expression in Mongolian gerbils
Author(s) -
Sugimoto Mitsushige,
Ohno Tomoyuki,
Graham David Y,
Yamaoka Yoshio
Publication year - 2011
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2011.06817.x
Subject(s) - helicobacter pylori , bacterial outer membrane , cytokine , microbiology and biotechnology , gastric mucosa , mutant , biology , inflammation , interleukin , immunology , medicine , stomach , gene , biochemistry , escherichia coli
Background and Aim: The levels of interleukin (IL)‐6 and IL‐11 in the gastric mucosa are related to mucosal inflammation; however, the chronological changes in cytokine expression during different phases of Helicobacter pylori infection and the effects of H. pylori virulence factors, particularly those of outer membrane proteins, remain obscure. The aim of this study was to clarify the chronological changes in cytokine levels in relation to several H. pylori outer membrane proteins. Methods: We studied Mongolian gerbils inoculated with wild‐type H . pylori 7.13 for up to 48 weeks and then examined animals infected with oipA , babA , or alpAB isogenic mutants for 12 weeks. Mucosal IL‐6 and IL‐11 mRNA levels were measured using real‐time reverse transcription‐polymerase chain reactions. Results: High levels of gastric mucosal IL‐6 and IL‐11 mRNA in gerbils infected with wild‐type H. pylori were observed during the chronic phase of infection, reaching maximums at 12 and 6 months, respectively. Infection with oipA and babA mutants resulted in significantly reduced cytokine levels and inflammatory cell infiltrations compared to gerbils infected with wild‐type strains, and this persisted throughout the observation period. The alpAB mutants did not infect gerbils. Mucosal IL‐6 and IL‐11 levels were significantly associated with the grade of inflammatory cell infiltration. Conclusions: OipA and BabA result in more severe H. pylori infection and increased IL‐6 and IL‐11 levels, which in turn may increase the risk of developing H. pylori ‐induced gastrointestinal diseases.