Journal of gastroenterology and hepatology · 2019
Duodenal and rectal mucosal microbiota related to small intestinal bacterial overgrowth in diarrhea-predominant irritable bowel syndrome.
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Yang Min, Zhang Lei, Hong Gaichao, Li Ying, Li Gangping, Qian Wei, Xiong Hanhua, Bai Tao, Song Jun, Hou Xiaohua
Аннотация
BACKGROUND AND AIM: Small intestinal bacterial overgrowth (SIBO) has been proposed as an etiologic factor in irritable bowel syndrome, particularly the diarrhea-predominant subtype (IBS-D). We aimed to identify potential intestinal microbial pattern in IBS-D patients with SIBO.
METHODS: Diarrhea-predominant irritable bowel syndrome patients fulfilling Rome III criteria were recruited and randomly divided into an exploratory cohort (57 cases) and a validation cohort (20 cases). SIBO was identified according to standard glucose hydrogen breath test. For 16S rRNA gene sequencing, samples of duodenal mucosa, duodenal fluid, rectal mucosa, and fresh feces were collected and performed. The α and β diversity, as well as differences in microbial composition and function, in SIBO+ and SIBO- IBS-D subjects were evaluated.
RESULTS: The microbial diversity and composition obviously differed between SIBO+ and SIBO- IBS-D in duodenal and rectal mucosa but not in duodenal fluid and fresh feces. For rectal mucosal microbiota, it displayed markedly reduced aerobe and Gram-negative bacteria and increased facultative anaerobe and Gram-positive bacteria, moreover, altered functions of microbial metabolism in SIBO+ IBS-D. Significantly higher rectal mucosa-related microbial dysbiosis index was observed in SIBO+ IBS-D, and a cut-off value at -0.37 had a sensitivity of 56.55% and specificity of 90.91% to identify the SIBO in IBS-D subjects.
CONCLUSIONS: Mucosal microbiota, rather than luminal bacteria, has a more apparent dysbiosis in SIBO+ IBS-D patients relative to those without SIBO. Rectal mucosa-associated microbiota may act as a potential predictor of SIBO in IBS-D patients.
METHODS: Diarrhea-predominant irritable bowel syndrome patients fulfilling Rome III criteria were recruited and randomly divided into an exploratory cohort (57 cases) and a validation cohort (20 cases). SIBO was identified according to standard glucose hydrogen breath test. For 16S rRNA gene sequencing, samples of duodenal mucosa, duodenal fluid, rectal mucosa, and fresh feces were collected and performed. The α and β diversity, as well as differences in microbial composition and function, in SIBO+ and SIBO- IBS-D subjects were evaluated.
RESULTS: The microbial diversity and composition obviously differed between SIBO+ and SIBO- IBS-D in duodenal and rectal mucosa but not in duodenal fluid and fresh feces. For rectal mucosal microbiota, it displayed markedly reduced aerobe and Gram-negative bacteria and increased facultative anaerobe and Gram-positive bacteria, moreover, altered functions of microbial metabolism in SIBO+ IBS-D. Significantly higher rectal mucosa-related microbial dysbiosis index was observed in SIBO+ IBS-D, and a cut-off value at -0.37 had a sensitivity of 56.55% and specificity of 90.91% to identify the SIBO in IBS-D subjects.
CONCLUSIONS: Mucosal microbiota, rather than luminal bacteria, has a more apparent dysbiosis in SIBO+ IBS-D patients relative to those without SIBO. Rectal mucosa-associated microbiota may act as a potential predictor of SIBO in IBS-D patients.