title: Protective effects of Lactobacillus rhamnosus [corrected] and Bifidobacterium infantis in murine models for colitis do not involve the vagus nerve.
abstract: The vagus nerve is an important pathway signaling immune activation of the gastrointestinal tract to the brain. Probiotics are live organisms that may engage signaling pathways of the brain-gut axis to modulate inflammation. The protective effects of Lactobacillus rhamnosus [corrected] (LR) and Bifidobacterium infantis (BI) during intestinal inflammation were studied after subdiaphragmatic vagotomy in acute dextran sulfate sodium (DSS) colitis in BALB/c mice and chronic colitis induced by transfer of CD4(+) CD62L(+) T lymphocytes from BALB/c into SCID mice. LR and BI (1 x 10(9)) were given daily. Clinical score, myeloperoxidase (MPO) levels, and in vivo and in vitro secreted inflammatory cytokine levels were found to be more severe in mice that were vagotomized compared with sham-operated animals. LR in the acute DSS model was effective in decreasing the MPO and cytokine levels in the tissue in sham and vagotomized mice. BI had a strong downregulatory effect on secreted in vitro cytokine levels and had a greater anti-inflammatory effect in vagotomized- compared with sham-operated mice. Both LR and BI retained anti-inflammatory effects in vagotomized mice. In SCID mice, vagotomy did not enhance inflammation, but BI was more effective in vagotomized mice than shams. Taken together, the intact vagus has a protective role in acute DSS-induced colitis in mice but not in the chronic T cell transfer model of colitis. Furthermore, LR and BI do not seem to engage their protective effects via this cholinergic anti-inflammatory pathway, but the results interestingly show that, in the T cell, transfer model vagotomy had a biological effect, since it increased the effectiveness of the BI in downregulation of colonic inflammation.
authors.affiliation: The Brain-Body Institute, St. Joseph's Healthcare Hamilton, Dept. of Pathology & Molecular Medicine, McMaster Univ., 50 Charlton Ave. East, Juravinski Innovation Tower, Rm. 3304, Hamilton, Ontario, Canada L8N 4A6.
authors.forename: Hanneke
authors.initials: H
authors.lastname: van der Kleij
authors.forename: Caitlin
authors.initials: C
authors.lastname: O'Mahony
authors.forename: Fergus
authors.initials: F
authors.lastname: Shanahan
authors.forename: Liam
authors.initials: L
authors.lastname: O'Mahony
authors.forename: John
authors.initials: J
authors.lastname: Bienenstock
mesh_terms: D000208:Acute Disease; D000284:Administration, Oral; D000818:Animals; D001644:Bifidobacterium / Q000502:physiology*; D001835:Body Weight / Q000187:drug effects; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology / Q000276:immunology; D002908:Chronic Disease; D003092:Colitis / Q000139:chemically induced / Q000276:immunology / Q000517:prevention & control*; D003106:Colon / Q000378:metabolism; D016264:Dextran Sulfate / Q000633:toxicity; D015850:Interleukin-6 / Q000378:metabolism; D052200:Limosilactobacillus reuteri / Q000502:physiology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D016513:Mice, SCID; D009195:Peroxidase / Q000378:metabolism; D019936:Probiotics / Q000008:administration & dosage / Q000627:therapeutic use*; D013154:Spleen / Q000166:cytology / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014628:Vagotomy; D014630:Vagus Nerve / Q000503:physiopathology / Q000601:surgery
chemical_list: D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016264:Dextran Sulfate; D009195:Peroxidase