Lessons learnt from post-infectious IBS

Sushil K. Sarna

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

The development of IBS symptoms - altered bowel function and abdominal cramping in a subset of adult subjects exposed to severe enteric infections opened up an unprecedented opportunity to understand the etiology of this poorly understood disorder. Perhaps, for the reasons that these symptoms follow a severe enteric infection, and mucosal biopsy tissues are readily available, the focus ofmost studies thus far has beento show that mild/low-grade mucosal inflammation persisting after the initial infection has subsided causes the IBS symptoms. Parallel studies in non-infectious IBS patients, who did not have prior enteritis, showed similar mild mucosal inflammation.Together, these studies examined the mucosal infiltration of specific immune cells, increase of select inflammatory mediators, mast cell and enterochromaffin cell hyperplasia, and epithelial permeability. In spite of the fact that the data on these topics were not consistent among different studies and clinical trials with prednisone, fluoxetine, and ketotifen failed to provide relief of IBS symptoms, the predominant conclusions were that mild mucosal inflammation is the cause of IBS symptoms. However, the circular smooth muscle cells, and myenteric neurons are the primary regulators of gut motility function, while primary afferent neurons and CNS play essential roles in induction of visceral hypersensitivity - no explanation was provided as to how mild mucosal inflammation causes dysfunction in cells far removed. Accumulating evidence shows that mild mucosal inflammation in IBS patients is in physiological range. It has little deleterious effects on cells within its own environment and therefore it is unlikely to affect cells in the muscularis externa. This review discusses the disconnect between the focus on mild/low-grade mucosal inflammation and the potential mechanisms and molecular dysfunctions in smooth muscle cells, myenteric neurons, and primary afferent neurons that may underlie IBS symptoms.

Original languageEnglish (US)
Article numberArticle 49
JournalFrontiers in Physiology
Volume2 AUG
DOIs
StatePublished - 2011

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Inflammation
Afferent Neurons
Smooth Muscle Myocytes
Infection
Enterochromaffin Cells
Ketotifen
Neurons
Enteritis
Fluoxetine
Prednisone
Mast Cells
Hyperplasia
Permeability
Hypersensitivity
Mucous Membrane
Clinical Trials
Biopsy

Keywords

  • Enteric neurons
  • Epithelial permeability
  • Functional bowel disorders
  • Gut inflammation
  • Immune cells
  • Inflammatory bowel disease
  • Smooth muscle
  • Visceral pain

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Lessons learnt from post-infectious IBS. / Sarna, Sushil K.

In: Frontiers in Physiology, Vol. 2 AUG, Article 49, 2011.

Research output: Contribution to journalArticle

Sarna, Sushil K. / Lessons learnt from post-infectious IBS. In: Frontiers in Physiology. 2011 ; Vol. 2 AUG.
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