Intestinal microbiota influences non-intestinal related autoimmune diseases

Maria C. Opazo, Elizabeth M. Ortega-Rocha, Irenice Coronado-Arrázola, Laura C. Bonifaz, Helene Boudin, Michel Neunlist, Susan M. Bueno, Alexis M. Kalergis, Claudia A. Riedel

Research output: Contribution to journalReview articlepeer-review

66 Citations (Scopus)

Abstract

The human body is colonized by millions of microorganisms named microbiota that interact with our tissues in a cooperative and non-pathogenic manner. These microorganisms are present in the skin, gut, nasal, oral cavities, and genital tract. In fact, it has been described that the microbiota contributes to balancing the immune system to maintain host homeostasis. The gut is a vital organ where microbiota can influence and determine the function of cells of the immune system and contributes to preserve the wellbeing of the individual. Several articles have emphasized the connection between intestinal autoimmune diseases, such as Crohn's disease with dysbiosis or an imbalance in the microbiota composition in the gut. However, little is known about the role of the microbiota in autoimmune pathologies affecting other tissues than the intestine. This article focuses on what is known about the role that gut microbiota can play in the pathogenesis of non-intestinal autoimmune diseases, such as Grave's diseases, multiple sclerosis, type-1 diabetes, systemic lupus erythematosus, psoriasis, schizophrenia, and autism spectrum disorders. Furthermore, we discuss as to how metabolites derived from bacteria could be used as potential therapies for non-intestinal autoimmune diseases.

Original languageEnglish
Article number432
JournalFrontiers in Microbiology
Volume9
Issue numberMAR
DOIs
Publication statusPublished - 12 Mar 2018

Keywords

  • Autoimmune disease
  • CNS
  • Gut
  • Microbiome
  • Microbiota
  • Skin

ASJC Scopus subject areas

  • Microbiology
  • Microbiology (medical)

Fingerprint

Dive into the research topics of 'Intestinal microbiota influences non-intestinal related autoimmune diseases'. Together they form a unique fingerprint.

Cite this