Gut 63:1737-1745 doi:10.1136/gutjnl-2013-305994
  • Neurogastroenterology
  • Original article

Faecal microbiota composition and host–microbe cross-talk following gastroenteritis and in postinfectious irritable bowel syndrome

  1. Willem M de Vos1,2,5
  1. 1Department of Veterinary Biosciences, Microbiology, University of Helsinki, Helsinki, Finland
  2. 2Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland
  3. 3NIHR Biomedical Research Unit, Nottingham Digestive Diseases Centre, University Hospital, Nottingham, UK
  4. 4GSK Research and Development Ltd, GlaxoSmithKline, Stevenage, UK
  5. 5Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands
  1. Correspondence to Jonna Jalanka-Tuovinen, Department of Veterinary Biosciences, University of Helsinki, PO Box 66, Helsinki FI-00014, Finland; Jonna.Jalanka{at}
  • Received 4 September 2013
  • Revised 22 October 2013
  • Accepted 11 November 2013
  • Published Online First 5 December 2013


Background About 10% of patients with IBS report the start of the syndrome after infectious enteritis. The clinical features of postinfectious IBS (PI-IBS) resemble those of diarrhoea-predominant IBS (IBS-D). While altered faecal microbiota has been identified in other IBS subtypes, composition of the microbiota in patients with PI-IBS remains uncharacterised.

Objective To characterise the microbial composition of patients with PI-IBS, and to examine the associations between the faecal microbiota and a patient's clinical features.

Design Using a phylogenetic microarray and selected qPCR assays, we analysed differences in the faecal microbiota of 57 subjects from five study groups: patients with diagnosed PI-IBS, patients who 6 months after gastroenteritis had either persisting bowel dysfunction or no IBS symptoms, benchmarked against patients with IBS-D and healthy controls. In addition, the associations between the faecal microbiota and health were investigated by correlating the microbial profiles to immunological markers, quality of life indicators and host gene expression in rectal biopsies.

Results Microbiota analysis revealed a bacterial profile of 27 genus-like groups, providing an Index of Microbial Dysbiosis (IMD), which significantly separated patient groups and controls. Within this profile, several members of Bacteroidetes phylum were increased 12-fold in patients, while healthy controls had 35-fold more uncultured Clostridia. We showed correlations between the IMD and expression of several host gene pathways, including amino acid synthesis, cell junction integrity and inflammatory response, suggesting an impaired epithelial barrier function in IBS.

Conclusions The faecal microbiota of patients with PI-IBS differs from that of healthy controls and resembles that of patients with IBS-D, suggesting a common pathophysiology. Moreover, our analysis suggests a variety of host–microbe associations that may underlie intestinal symptoms, initiated by gastroenteritis.