Postinfection Irritable Bowel Syndrome: The Links between Gastroenteritis, Inflammation, the Microbiome, and Functional Disease

Research output: Contribution to journalReview article

8 Citations (Scopus)

Abstract

Postinfection irritable bowel syndrome (PI-IBS) is a diarrheal disease that develops after infectious gastroenteritis (IGE). Profound alterations in the microbiota accompany IGE yet only 10% of IGE patients progress to PI-IBS. This review explores research linking IGE severity, psychological comorbidity, PI-IBS, and the microbiome in various patient populations. Selective pressures caused by inflammation and increased gastrointestinal motility during gastroenteritis can alter intestinal bacterial phyla including Bacteroidetes, Firmicutes, and Proteobacteria. More specifically, classes such as Bacteroides and Clostridia are differentially abundant in many PI-IBS patients. Altered microbiota may perpetuate a cycle of enteric and systemic inflammation, potently activating neural afferent signaling in the enteric nervous system and causing pain and diarrhea in PI-IBS patients. Altered production of microbial metabolites, for example short chain fatty acids, may have enteric and systemic effects on the host. Longitudinal sampling to characterize changes in the microbiota's genetic, metabolic, and transcriptional activities over time from IGE to PI-IBS may enable improved diagnosis and classification of PI-IBS cases into subtypes, allowing for targeted antibiotic, probiotic, and prebiotic treatments. PI-IBS is a heterogenous and largely organic disease marked by specific alterations in functions of the microbiota and is an important model for studying microbial influences on intestinal, neurological, and psychological host functions.

Original languageEnglish (US)
Pages (from-to)869-877
Number of pages9
JournalJournal of Clinical Gastroenterology
Volume51
Issue number10
DOIs
StatePublished - 2017

Fingerprint

Irritable Bowel Syndrome
Microbiota
Gastroenteritis
Inflammation
Bacteroidetes
Psychology
Enteric Nervous System
Proteobacteria
Prebiotics
Bacteroides
Gastrointestinal Motility
Clostridium
Volatile Fatty Acids
Probiotics
Comorbidity
Diarrhea
Anti-Bacterial Agents
Pain
Research

Keywords

  • Barrier function
  • Diarrhea-predominant irritable bowel syndrome
  • Infectious gastroenteritis
  • Microbiome
  • Postinfection syndrome

ASJC Scopus subject areas

  • Gastroenterology

Cite this

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title = "Postinfection Irritable Bowel Syndrome: The Links between Gastroenteritis, Inflammation, the Microbiome, and Functional Disease",
abstract = "Postinfection irritable bowel syndrome (PI-IBS) is a diarrheal disease that develops after infectious gastroenteritis (IGE). Profound alterations in the microbiota accompany IGE yet only 10{\%} of IGE patients progress to PI-IBS. This review explores research linking IGE severity, psychological comorbidity, PI-IBS, and the microbiome in various patient populations. Selective pressures caused by inflammation and increased gastrointestinal motility during gastroenteritis can alter intestinal bacterial phyla including Bacteroidetes, Firmicutes, and Proteobacteria. More specifically, classes such as Bacteroides and Clostridia are differentially abundant in many PI-IBS patients. Altered microbiota may perpetuate a cycle of enteric and systemic inflammation, potently activating neural afferent signaling in the enteric nervous system and causing pain and diarrhea in PI-IBS patients. Altered production of microbial metabolites, for example short chain fatty acids, may have enteric and systemic effects on the host. Longitudinal sampling to characterize changes in the microbiota's genetic, metabolic, and transcriptional activities over time from IGE to PI-IBS may enable improved diagnosis and classification of PI-IBS cases into subtypes, allowing for targeted antibiotic, probiotic, and prebiotic treatments. PI-IBS is a heterogenous and largely organic disease marked by specific alterations in functions of the microbiota and is an important model for studying microbial influences on intestinal, neurological, and psychological host functions.",
keywords = "Barrier function, Diarrhea-predominant irritable bowel syndrome, Infectious gastroenteritis, Microbiome, Postinfection syndrome",
author = "Downs, {Ian A.} and Aroniadis, {Olga C.} and Libusha Kelly and Brandt, {Lawrence J.}",
year = "2017",
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TY - JOUR

T1 - Postinfection Irritable Bowel Syndrome

T2 - The Links between Gastroenteritis, Inflammation, the Microbiome, and Functional Disease

AU - Downs, Ian A.

AU - Aroniadis, Olga C.

AU - Kelly, Libusha

AU - Brandt, Lawrence J.

PY - 2017

Y1 - 2017

N2 - Postinfection irritable bowel syndrome (PI-IBS) is a diarrheal disease that develops after infectious gastroenteritis (IGE). Profound alterations in the microbiota accompany IGE yet only 10% of IGE patients progress to PI-IBS. This review explores research linking IGE severity, psychological comorbidity, PI-IBS, and the microbiome in various patient populations. Selective pressures caused by inflammation and increased gastrointestinal motility during gastroenteritis can alter intestinal bacterial phyla including Bacteroidetes, Firmicutes, and Proteobacteria. More specifically, classes such as Bacteroides and Clostridia are differentially abundant in many PI-IBS patients. Altered microbiota may perpetuate a cycle of enteric and systemic inflammation, potently activating neural afferent signaling in the enteric nervous system and causing pain and diarrhea in PI-IBS patients. Altered production of microbial metabolites, for example short chain fatty acids, may have enteric and systemic effects on the host. Longitudinal sampling to characterize changes in the microbiota's genetic, metabolic, and transcriptional activities over time from IGE to PI-IBS may enable improved diagnosis and classification of PI-IBS cases into subtypes, allowing for targeted antibiotic, probiotic, and prebiotic treatments. PI-IBS is a heterogenous and largely organic disease marked by specific alterations in functions of the microbiota and is an important model for studying microbial influences on intestinal, neurological, and psychological host functions.

AB - Postinfection irritable bowel syndrome (PI-IBS) is a diarrheal disease that develops after infectious gastroenteritis (IGE). Profound alterations in the microbiota accompany IGE yet only 10% of IGE patients progress to PI-IBS. This review explores research linking IGE severity, psychological comorbidity, PI-IBS, and the microbiome in various patient populations. Selective pressures caused by inflammation and increased gastrointestinal motility during gastroenteritis can alter intestinal bacterial phyla including Bacteroidetes, Firmicutes, and Proteobacteria. More specifically, classes such as Bacteroides and Clostridia are differentially abundant in many PI-IBS patients. Altered microbiota may perpetuate a cycle of enteric and systemic inflammation, potently activating neural afferent signaling in the enteric nervous system and causing pain and diarrhea in PI-IBS patients. Altered production of microbial metabolites, for example short chain fatty acids, may have enteric and systemic effects on the host. Longitudinal sampling to characterize changes in the microbiota's genetic, metabolic, and transcriptional activities over time from IGE to PI-IBS may enable improved diagnosis and classification of PI-IBS cases into subtypes, allowing for targeted antibiotic, probiotic, and prebiotic treatments. PI-IBS is a heterogenous and largely organic disease marked by specific alterations in functions of the microbiota and is an important model for studying microbial influences on intestinal, neurological, and psychological host functions.

KW - Barrier function

KW - Diarrhea-predominant irritable bowel syndrome

KW - Infectious gastroenteritis

KW - Microbiome

KW - Postinfection syndrome

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