Gastroenterol Clin North Am. 2021 Jun;50(2):445-461.doi: 10.1016/j.gtc.2021.02.007. Epub 2021 Apr 23.

Antonio Berumen ¹, Adam L Edwinson ¹, Madhusudan Grover ²

Author information

• ¹Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, USA.
• ²Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, USA; Department of Medicine and Physiology, Enteric NeuroScience Program, 200 First Street Southwest, Rochester, MN 55905, USA. Electronic address: grover.madhusudan@mayo.edu.

Abstract

Epidemiologic data support that acute gastrointestinal infection is one of the strongest risk factors for development of irritable bowel syndrome (IBS). Risk of post-infection IBS (PI-IBS) seems to be greater with bacterial and protozoal than viral enterocolitis. Younger individuals, women, and those with severe enterocolitis are more likely to develop PI-IBS. Disease mechanisms in animal models and humans involve chronic perturbation of intestinal microbiome, epithelial and neuronal remodeling, and immune activation. These mechanisms can lead to luminal (increased proteolytic activity, altered bile acid composition) and physiologic (increased permeability, transit changes, and visceral hypersensitivity) alterations that can mediate PI-IBS symptoms.