title: Inflammation and foveolar hyperplasia are reduced by supplemental dietary glutamine during Helicobacter pylori infection in mice.
abstract: 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-1beta 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.
authors.affiliation: Department of Surgery, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. shagen@bidmc.harvard.edu
authors.forename: Susan J
authors.initials: SJ
authors.lastname: Hagen
authors.forename: Masa
authors.initials: M
authors.lastname: Ohtani
authors.forename: Jin-Rong
authors.initials: JR
authors.lastname: Zhou
authors.forename: Nancy S
authors.initials: NS
authors.lastname: Taylor
authors.forename: Barry H
authors.initials: BH
authors.lastname: Rickman
authors.forename: George L
authors.initials: GL
authors.lastname: Blackburn
authors.forename: James G
authors.initials: JG
authors.lastname: Fox
mesh_terms: D000818:Animals; D004032:Diet; D019587:Dietary Supplements; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology*; D005756:Gastritis / Q000382:microbiology / Q000517:prevention & control*; D005973:Glutamine / Q000008:administration & dosage*; D016481:Helicobacter Infections / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D016480:Helicobacter pylori / Q000254:growth & development; D006965:Hyperplasia; D007074:Immunoglobulin G / Q000097:blood; D051379:Mice; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013270:Stomach / Q000737:chemistry / Q000382:microbiology / Q000473:pathology
chemical_list: D007074:Immunoglobulin G; D012333:RNA, Messenger; D005973:Glutamine