J Neurogastroenterol Motil.  2012 Jul;18(3):258-268.

An Update on Post-infectious Irritable Bowel Syndrome: Role of Genetics, Immune Activation, Serotonin and Altered Microbiome

Affiliations
  • 1NIHR Biomedical Research Unit in the Nottingham Digestive Diseases Centre, Nottingham, United Kingdom. robin.spiller@nottingham.ac.uk

Abstract

The literature on post-infectious irritable bowel syndrome (IBS) is reviewed with special emphasis on recent new data. Further accounts of this phenomenon continue to be reported following a range of infections including giardiasis as well as viral and bacterial gastroenteritis. Risk factors such as severity of initial illness, female gender together with adverse psychological factors have been confirmed. Recent evidence of a genetic predisposition needs replication. Animal studies suggest activation of mast cells and inflammation driven impairment of serotonin transporter may be important, which are findings supported by some recent human studies in IBS with diarrhoea. Experimentally induced inflammation leads to damage and remodelling of enteric nerves. Similar changes have been reported in IBS patients with increase in nerves expressing transient receptor potential cation channel V1. While changes in microbiota are very likely this area has yet to be explored using modern techniques. Since the prognosis is for slow improvement, treatments should currently target the key symptoms of diarrhoea and abdominal pain. Future therapies aimed at correcting underlying mechanisms including immune activation and serotonin excess are currently being explored and may provide better treatments in the future.

Keyword

Genetics; Infection; Irritable bowel syndrome; Serotonin

MeSH Terms

Abdominal Pain
Animals
Female
Gastroenteritis
Genetic Predisposition to Disease
Giardiasis
Humans
Inflammation
Irritable Bowel Syndrome
Mast Cells
Metagenome
Prognosis
Risk Factors
Serotonin
Serotonin Plasma Membrane Transport Proteins
Serotonin
Serotonin Plasma Membrane Transport Proteins
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