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Dietary glutamine supplementation reduces inflammation and hyperplasia during Helicobacter pylori infection in the mouse stomach
Author(s) -
Hagen Susan J.,
Ohtani Masahiro,
Zhou JinRong,
Blackburn George L.,
Taylor Nancy S.,
Rickman Barry,
Fox James G.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.939.4
Subject(s) - glutamine , inflammation , stomach , gut flora , atrophy , hyperplasia , medicine , helicobacter pylori , gastritis , intestinal metaplasia , immunology , gastroenterology , endocrinology , biology , biochemistry , amino acid
Glutamine (GLN) protects cultured gastric mucosal cells against injury. The purpose of this study was to test whether dietary GLN supplementation protects gastric mucosal cells against injury in vivo . METHODS C57BL/6 mice were fed a purified test diet without or with 5% GLN and, after 2 weeks of pre‐feeding, were sham‐ or Helicobacter pylori (HP‐SS1)‐infected. Body weight and food consumption were recorded and tissues were analyzed for pathology at 6, 12, and 20 weeks post‐infection (WPI). HP colonization and the level of pro‐ or anti‐inflammatory cytokines were determined by quantitative RT‐PCR. RESULTS GLN supplementation resulted in a robust early (6 WPI) inflammatory response to HP followed by a significant reduction in inflammation by 20 WPI. Hyperplasia was notable by 12 WPI on either diet but decreased significantly with GLN by 20 WPI. There was a robust anti‐inflammatory response with GLN, consisting of a significant increase in IL‐4, IL‐10, and TGF‐β at 6 WPI. After this initial response, there was a reduction or no change in anti‐inflammatory mRNA levels over time. Food consumption and HP colonization were not different in mice fed the GLN diet nor was there a significant change in atrophy or metaplasia scores. CONCLUSIONS Our results demonstrate that supplemental dietary GLN reduces inflammation and hyperplasia during HP‐infection in the mouse stomach. Supported by R01 DK15681 from the NIH.