Author information

1 Division of Gastroenterology and Hepatology, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, 7340 MBRB Building, 111 Mason Farm Road, Chapel Hill, NC, 27599, USA.

2 Bacteriotherapy Clinic, Department of Gastroenterology and Liver Diseases, Tel Aviv Medical Center Affiliated with the Sackler Faculty of Medicine, Tel Aviv University, 6 Weizmann St., Tel Aviv, Israel.

3 Division of Gastroenterology and Hepatology, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, 7340 MBRB Building, 111 Mason Farm Road, Chapel Hill, NC, 27599, USA. udiringel@clalit.org.il.

4 Department of Gastroenterology and Hepatology, Meir Medical Center, Affiliated with Tel Aviv University, 59 Tshernichovsky St., 4428164, Kfar Saba, Israel. udiringel@clalit.org.il.

5 Division of Gastroenterology and Hepatology, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, 7309A MBRB Building, 111 Mason Farm Road, Chapel Hill, NC, 27599, USA.

6 Department of Maternal and Child Health, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, 404A Rosenau, Chapel Hill, NC, 27599, USA.

Abstract

BACKGROUND: Irritable bowel syndrome (IBS) has been associated with changes in the intestinal microbiota. Only a few studies have explored differences in the mucosa-associated microbiota between IBS patients and healthy controls (HC).

AIMS: To characterize and compare the microbiota in mucosal and fecal samples from carefully selected patients with IBS-D and HC.

METHODS: The cohort was composed of 23 diarrhea-predominant IBS (IBS-D) patients and 24 HC. Fresh stool samples were collected from participants prior to the collection of colonic mucosal samples from an unprepped bowel. After DNA extraction, 16S rRNA genes were sequenced by 454 pyrosequencing and analyzed using the QIIME pipeline.

RESULTS: The fecal microbiota (luminal niche) of IBS-D patients was found to have reduced enteric richness compared to HC (P < 0.05), whereas no differences were observed between the two groups within the mucosal microbiota. Within the luminal niche, the relative proportions of Faecalibacterium genus were found to be lower in IBS-D than in HC and the Dorea genus was higher in IBS-D. None of the taxa proportions were significantly different in IBS-D patients versus HC using an FDR of ≤ 0.1 when analyzing samples that appeared in > 25% samples of either niche.

CONCLUSION: Fecal and mucosal microbiota of IBS-D patients and HC are very similar and are not sufficient to explain the reported altered physiology and symptomatology of IBS-D. Future studies should investigate intestinal microbiome-dependent functional activity in addition to the fecal and mucosal-associated microbial composition.