Inflammation and Foveolar Hyperplasia Are Reduced by Supplemental Dietary Glutamine during Helicobacter pylori Infection in Mice1–3

We recently showed that L-Gln protects cultured gastric cells from ammonia-induced cell death and predicted that Gln may also protect during Helicobacter pylori infection in vivo. Thus, the aim of this study was to test whether supplemental dietary Gln protects against H. pylori-associated pathology...

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Published inThe Journal of nutrition Vol. 139; no. 5; pp. 912 - 918
Main Authors Hagen, Susan J., Ohtani, Masa, Zhou, Jin-Rong, Taylor, Nancy S., Rickman, Barry H., Blackburn, George L., Fox, James G.
Format Journal Article
LanguageEnglish
Published Bethesda Elsevier Inc 01.05.2009
American Institute of Nutrition
American Society for Nutrition
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Summary:We recently showed that L-Gln protects cultured gastric cells from ammonia-induced cell death and predicted that Gln may also protect during Helicobacter pylori infection in vivo. Thus, the aim of this study was to test whether supplemental dietary Gln protects against H. pylori-associated pathology. For this, C57BL/6 mice were fed a purified diet consisting of 20.3% protein (1.9% Gln), 66% carbohydrate, and 5% fat or 25.3% protein (5% supplemental L-Gln; 6.9% total Gln), 61% carbohydrate, and 5% fat. After a 2-wk prefeeding period, mice were divided into sham-(uninfected) or H. pylori-infected groups. Body weight and food consumption were recorded weekly. Tissue histopathology, H. pylori colonization, serum IgG, and pro- and antiinflammatory cytokine mRNA expression were determined at 6, 12, and 20 wk postinfection (wkPI). Inflammation, antiinflammatory cytokine, and interleukin-1β mRNA expression were significantly greater at 6 wkPI in H. pylori-infected mice fed supplemental Gln compared with those fed the control diet. At 20 wkPI, however, inflammation and foveolar hyperplasia were significantly lower in H. pylori-infected mice fed supplemental Gln compared with those fed the control diet. Body weight gain, food consumption, H. pylori colonization, and serum IgG did not differ in H. pylori-infected mice fed supplemental Gln compared with the control diet. Our data demonstrate that H. pylori-infected mice fed supplemental dietary Gln have reduced H. pylori-associated pathology in vivo that is accompanied by beneficial changes in the immune response to H. pylori early in infection. Thus, Gln supplementation may be an alternative therapy for reducing H. pylori-associated pathology.
Bibliography:To whom correspondence should be addressed. E-mail: shagen@bidmc.harvard.edu.
Supplemental Figure 1 is available with the online posting of this paper at jn.nutrition.org.
Author disclosures: S. J. Hagen was provided honoraria and paid travel expenses by the Ajinomoto and Kotobuki Pharmaceutical Companies for speaking at meetings or giving lectures about data concerning glutamine. M. Ohtani, J.-R. Zhou, N. S. Taylor, B. H. Rickman, G. L. Blackburn, and J. G. Fox, no conflicts of interest.
Abbreviations used: GAPDH, glyceraldehyde 3-phosphate dehydrogenase; HPCont; Helicobacter pylori-infected mice fed a control diet; HPGln, Helicobacter pylori-infected mice fed a Gln-supplemented diet; IL, interleukin; SS1, Helicobacter pylori Sydney strain 1; TH, T-helper; TGFβ, transforming growth factor-β; UCont, uninfected mice fed a control diet; UGln, uninfected mice fed a Gln-supplemented diet; wkPI, week postinfection.
Supported by the NIH grants R01 DK-15681 (S. J. Hagen), P30 DK-34854 (Harvard Digestive Diseases Center), R01 CA-67463, and AI/RR-37750 (J. G. Fox).
ISSN:0022-3166
1541-6100
DOI:10.3945/jn.108.097790