Homeostasis and Dysbiosis of the Intestinal Microbiota: Comparing Hallmarks of a Healthy State with Changes in Inflammatory Bowel Disease

Microorganisms. 2022 Dec 5;10(12):2405. doi: 10.3390/microorganisms10122405.

Abstract

The gut microbiota, which represent a community of different microorganisms in the human intestinal tract, are crucial to preserving human health by participating in various physiological functions and acting as a metabolic organ. In physiological conditions, microbiota-host partnership exerts homeostatic stability; however, changes in intestinal microbiota composition (dysbiosis) are an important factor in the pathogenesis of inflammatory bowel disease and its two main disease entities: ulcerative colitis and Crohn's disease. The incidence and prevalence of these inflammatory conditions have increased rapidly in the last decade, becoming a significant problem for the healthcare system and a true challenge in finding novel therapeutic solutions. The issue is that, despite numerous studies, the etiopathogenesis of inflammatory bowel disease is not completely clear. Based on current knowledge, chronic intestinal inflammation occurs due to altered intestinal microbiota and environmental factors, as well as a complex interplay between the genetic predisposition of the host and an inappropriate innate and acquired immune response. It is important to note that the development of biological and immunomodulatory therapy has led to significant progress in treating inflammatory bowel disease. Certain lifestyle changes and novel approaches-including fecal microbiota transplantation and nutritional supplementation with probiotics, prebiotics, and synbiotics-have offered solutions for dysbiosis management and paved the way towards restoring a healthy microbiome, with only minimal long-term unfavorable effects.

Keywords: Crohn’s disease; dysbiosis; inflammatory bowel disease; microbiome; microbiota; nutrition; ulcerative colitis.

Publication types

  • Review

Grants and funding

This research received no external funding.