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Commensal microbiota induces colonic barrier structure and functions that contribute to homeostasis.

Christina L Hayes | Jasmine Dong | Heather J Galipeau | Jennifer Jury | Justin McCarville | Xianxi Huang | Xuan-Yu Wang | Avee Naidoo | Arivarasu N Anbazhagan | Josie Libertucci | Conor Sheridan | Pradeep K Dudeja | Dawn M E Bowdish | Michael G Surette | Elena F Verdu
Scientific reports | 2018

The intestinal barrier encompasses structural, permeability and immune aspects of the gut mucosa that, when disrupted, may contribute to chronic inflammation. Although gnotobiotic studies have demonstrated the effects of microbiota on mucosal and systemic immunity, as well as intestinal barrier architecture and innate immune characteristics, its impact on barrier function remains unclear. We compared germ-free and conventional mice, as well as mice colonized with human fecal microbiota that were followed for 21 days post-colonization. Colonic barrier structure was investigated by immunohistochemistry, molecular and electron microscopy techniques. Permeability was assessed in colon tissue by Ussing chambers, and by serum LPS and MDP detection using TLR4- and NOD2-NFκB reporter assays. Microbiota profile was determined by Illumina 16S rRNA gene sequencing. Low dose dextran sodium sulfate was administered to assess microbiota-induced barrier changes on resistance to colonic injury. Permeability to paracellular probes and mucus layer structure resembled that of conventional mice by day 7 post-colonization, coinciding with reduced claudin-1 expression and transient IL-18 production by intestinal epithelial cells. These post-colonization adaptations were associated with decreased systemic bacterial antigen exposure and reduced susceptibility to intestinal injury. In conclusion, commensal colonization promotes physiological barrier structural and functional adaptations that contribute to intestinal homeostasis.

Pubmed ID: 30242285

Associated grants

  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK054016
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK092441

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

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