The Intersection of TNF, IBD and the Microbiome

Gut Microbes. 2016;7(1):58-62. doi: 10.1080/19490976.2015.1121364.

Abstract

Inflammatory bowel disease (IBD), comprised of Crohn's disease and ulcerative colitis, is a chronic inflammatory condition of multifactorial etiology and risk factors. Currently, one of the most effective treatments for IBD is the use of Tumor Necrosis Factor (TNF) functional inhibitor drugs, however, this treatment can cause adverse reactions and has a relatively large percentage of incomplete or non-responders. This lack of response may be related to differences in patients' gut microbiomes prior to and after disease initiation or treatment. Recent observations in our lab using a rodent model of IBD support the theory that TNF drives acute colitis, but also that the microbiome differs in association with TNF production and colitis severity. Studies such as this and others provide new insights into host-microbiome interactions associated with colitis that can lead to new therapies to prevent or treat the disease.

Keywords: TNBS; colitis; inflammatory bowel disease; microbiota; mouse model; tumor necrosis factor.

MeSH terms

  • Animals
  • CD4-Positive T-Lymphocytes / immunology*
  • Colitis, Ulcerative / drug therapy*
  • Colitis, Ulcerative / pathology*
  • Crohn Disease / drug therapy*
  • Crohn Disease / pathology*
  • Cytokines / immunology*
  • Disease Models, Animal
  • Firmicutes / pathogenicity
  • Gastrointestinal Microbiome / immunology*
  • Humans
  • Immunity, Mucosal / immunology
  • Mice
  • Symbiosis / immunology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*

Substances

  • Cytokines
  • TNF protein, human
  • Tumor Necrosis Factor-alpha