Partners in Leaky Gut Syndrome: Intestinal Dysbiosis and Autoimmunity

Yusuke Kinashi, Koji Hase

Research output: Contribution to journalReview articlepeer-review

110 Citations (Scopus)


The intestinal surface is constitutively exposed to diverse antigens, such as food antigens, food-borne pathogens, and commensal microbes. Intestinal epithelial cells have developed unique barrier functions that prevent the translocation of potentially hostile antigens into the body. Disruption of the epithelial barrier increases intestinal permeability, resulting in leaky gut syndrome (LGS). Clinical reports have suggested that LGS contributes to autoimmune diseases such as type 1 diabetes, multiple sclerosis, rheumatoid arthritis, and celiac disease. Furthermore, the gut commensal microbiota plays a critical role in regulating host immunity; abnormalities of the microbial community, known as dysbiosis, are observed in patients with autoimmune diseases. However, the pathological links among intestinal dysbiosis, LGS, and autoimmune diseases have not been fully elucidated. This review discusses the current understanding of how commensal microbiota contributes to the pathogenesis of autoimmune diseases by modifying the epithelial barrier.

Original languageEnglish
Article number673708
JournalFrontiers in Immunology
Publication statusPublished - 2021 Apr 22


  • autoimmune diseases
  • dysbiosis
  • epithelial barrier
  • gut immune system
  • leaky gut syndrome
  • microbiota

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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