title: Lactobacillus rhamnosus CNCM I-3690 and the commensal bacterium Faecalibacterium prausnitzii A2-165 exhibit similar protective effects to induced barrier hyper-permeability in mice.
abstract: Impaired gut barrier function has been reported in a wide range of diseases and syndromes and in some functional gastrointestinal disorders. In addition, there is increasing evidence that suggests the gut microbiota tightly regulates gut barrier function and recent studies demonstrate that probiotic bacteria can enhance barrier integrity. Here, we aimed to investigate the effects of Lactobacillus rhamnosus CNCM I-3690 on intestinal barrier function. In vitro results using a Caco-2 monolayer cells stimulated with TNF-α confirmed the anti-inflammatory nature of the strain CNCM I-3690 and pointed out a putative role for the protection of the epithelial function. Next, we tested the protective effects of L. rhamnosus CNCM I-3690 in a mouse model of increased colonic permeability. Most importantly, we compared its performance to that of the well-known beneficial human commensal bacterium Faecalibacterium prauznitzii A2-165. Increased colonic permeability was normalized by both strains to a similar degree. Modulation of apical tight junction proteins expression was then analyzed to decipher the mechanism underlying this effect. We showed that CNCM I-3690 partially restored the function of the intestinal barrier and increased the levels of tight junction proteins Occludin and E-cadherin. The results indicate L. rhamnosus CNCM I-3690 is as effective as the commensal anti-inflammatory bacterium F. prausnitzii to treat functional barrier abnormalities.
authors.affiliation: a INRA ; Commensal and Probiotics-Host Interactions Laboratory ; UMR 1319 Micalis ; F-78350; Jouy-en-Josas , France.
authors.forename: L
authors.initials: L
authors.lastname: Laval
authors.forename: R
authors.initials: R
authors.lastname: Martin
authors.forename: J N
authors.initials: JN
authors.lastname: Natividad
authors.forename: F
authors.initials: F
authors.lastname: Chain
authors.forename: S
authors.initials: S
authors.lastname: Miquel
authors.forename: C
authors.initials: C
authors.lastname: Desclée de Maredsous
authors.forename: S
authors.initials: S
authors.lastname: Capronnier
authors.forename: H
authors.initials: H
authors.lastname: Sokol
authors.forename: E F
authors.initials: EF
authors.lastname: Verdu
authors.forename: J E T
authors.initials: JE
authors.lastname: van Hylckama Vlieg
authors.forename: L G
authors.initials: LG
authors.lastname: Bermúdez-Humarán
authors.forename: T
authors.initials: T
authors.lastname: Smokvina
authors.forename: P
authors.initials: P
authors.lastname: Langella
mesh_terms: D032761:Animal Experimentation; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage*; D018938:Caco-2 Cells; D003013:Clostridium / Q000254:growth & development / Q000502:physiology*; D004847:Epithelial Cells / Q000187:drug effects / Q000382:microbiology; D020869:Gene Expression Profiling; D006801:Humans; D007413:Intestinal Mucosa / Q000187:drug effects / Q000502:physiology*; D052201:Lacticaseibacillus rhamnosus / Q000254:growth & development / Q000502:physiology*; D008297:Male; D008810:Mice, Inbred C57BL; D010539:Permeability / Q000187:drug effects*; D019936:Probiotics / Q000008:administration & dosage*; D062725:Tight Junction Proteins / Q000096:biosynthesis; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D062725:Tight Junction Proteins; D014409:Tumor Necrosis Factor-alpha
keywords: AJs, adherence junctions; CNCM, Collection Nationale de Cultures de Microorganismes; DNBS, DiNitroBenzene Sulfonic; EOS, extremely oxygen sensitive; GVHD, graft-versus-host disease; IBD, inflammatory bowel diseases; IBS, irritable bowel syndrome; LAB, lac; apical junction proteins; lactobacilli; probiotics