title: Specific changes of gut commensal microbiota and TLRs during indomethacin-induced acute intestinal inflammation in rats.
abstract: OBJECTIVE
  Gut microbiota is a contributing factor in the development and maintenance of intestinal inflammation, although precise cause-effect relationships have not been established. We assessed spontaneous changes of gut commensal microbiota and toll-like receptors (TLRs)-mediated host-bacterial interactions in a model of indomethacin-induced acute enteritis in rats.
  
  
  METHODS
  Male Spague-Dawley rats, maintained under conventional conditions, were used. Enteritis was induced by systemic indomethacin administration. During the acute phase of inflammation, animals were euthanized and ileal and ceco-colonic changes evaluated. Inflammation was assessed through disease activity parameters (clinical signs, macroscopic/microscopic scores and tissue levels of inflammatory markers). Microbiota (ileal and ceco-colonic) was characterized using fluorescent in situ hybridization (FISH) and analysis of 16s rDNA polymorphism. Host-bacterial interactions were assessed evaluating the ratio of bacterial adherence to the intestinal wall (FISH) and expression of TLRs 2 and 4 (RT-PCR).
  
  
  RESULTS
  After indomethacin, disease activity parameters increased, suggesting an active inflammation. Total bacterial counts were similar in vehicle- or indomethacin-treated animals. However, during inflammation the relative composition of the microbiota was altered. This dysbiotic state was characterized by an increase in the counts of Bacteroides spp., Enterobacteriaceae (in ileum and cecum-colon) and Clostridium spp. (in ileum). Bacterial wall adherence significantly increased during inflammation. In animals with enteritis, TLR-2 and -4 were up-regulated both in the ileum and the ceco-colonic region.
  
  
  CONCLUSIONS
  Gut inflammation implies qualitative changes in GCM, with simultaneous alterations in host-bacterial interactions. These observations further support a potential role for gut microbiota in the pathophysiology of intestinal inflammation.
authors.affiliation: Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Barcelona, Spain.
authors.forename: Evangelina
authors.initials: E
authors.lastname: Terán-Ventura
authors.affiliation: Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Barcelona, Spain; Neuroscience Institute, Universitat Autònoma de Barcelona, Barcelona, Spain.
authors.forename: Mònica
authors.initials: M
authors.lastname: Aguilera
authors.affiliation: Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Barcelona, Spain; Neuroscience Institute, Universitat Autònoma de Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain.
authors.forename: Patri
authors.initials: P
authors.lastname: Vergara
authors.affiliation: Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Barcelona, Spain; Neuroscience Institute, Universitat Autònoma de Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Spain. Electronic address: vicente.martinez@uab.es.
authors.forename: Vicente
authors.initials: V
authors.lastname: Martínez
mesh_terms: D000818:Animals; D001422:Bacterial Adhesion; D004195:Disease Models, Animal; D007213:Indomethacin / Q000633:toxicity; D015212:Inflammatory Bowel Diseases / Q000139:chemically induced / Q000378:metabolism / Q000382:microbiology*; D007413:Intestinal Mucosa / Q000378:metabolism / Q000382:microbiology*; D008297:Male; D064307:Microbiota / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D051193:Toll-Like Receptors / Q000378:metabolism*
chemical_list: D051193:Toll-Like Receptors; D007213:Indomethacin
keywords: Bacterial adherence; FISH; Gut commensal microbiota; Gut inflammation; Host–bacterial interactions; Inflammatory bowel disease; TLR; Toll-like receptors