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Effect of altered gut microbiota on visceral hypersensitivity of postinfectious irritable bowel syndrome mice.
Eur J Gastroenterol Hepatol. 2022 12 01; 34(12):1220-1230.EJ

Abstract

OBJECTIVE

Irritable bowel syndrome (IBS) is a common functional bowel disorder characterized with visceral hypersensitivity. Previous studies indicated gut microbiota alteration associated short-chain fatty acids (SCFAs) dysregulation is associated with IBS development. The aim of the study is to explore the potential role of microbiota dysbiosis mediated visceral hypersensitivity in postinfectious-IBS (PI-IBS) mouse model.

METHODS

Four-week-old NIH mice were randomly allocated into four groups: control mice, PI-IBS mice, PI-IBS mice co-housing with normal mice, and PI-IBS mice were administrated with a cocktail of antibiotics. Trichinella spiralis infection established PI-IBS mouse model. Microbiota in cecal contents and feces were analyzed by 16S rDNA sequencing. SCFAs were detected by gas chromatography. 5-hydroxytryptamine (5-HT) was evaluated by ELISA, and N-methyl-D-aspartate receptors (NMDARs) were examined by western blot. Visceral sensitivity was determined by abdominal withdrawal reflex in response to colorectal distention.

RESULTS

Increased SCFAs were observed in cecal contents and feces in PI-IBS mice accompanied with higher 5-HT and NMDAR subunits expressions in ileum and colon. Visceral hypersensitivity was observed in PI-IBS mice compared to control mice. When administrated with antibiotics cocktails and co-housing with normal mice, PI-IBS mice showed decreased SCFAs, 5-HT, NMDAR subunits expressions, and improved visceral hypersensitivity.

CONCLUSION

Gut microbiota alteration induced increased SCFAs, 5-HT and NMDAR subunits expressions were associated with visceral hypersensitivity in PI-IBS mice. The critical role of gut microbiota in improving visceral hypersensitivity was further identified by treatment of antibiotics cocktail and co-housing.

Authors+Show Affiliations

Department of Gastroenterology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

36165068

Citation

Cheng, Fangli, et al. "Effect of Altered Gut Microbiota On Visceral Hypersensitivity of Postinfectious Irritable Bowel Syndrome Mice." European Journal of Gastroenterology & Hepatology, vol. 34, no. 12, 2022, pp. 1220-1230.
Cheng F, Fan Z, Lin C, et al. Effect of altered gut microbiota on visceral hypersensitivity of postinfectious irritable bowel syndrome mice. Eur J Gastroenterol Hepatol. 2022;34(12):1220-1230.
Cheng, F., Fan, Z., Lin, C., Zhu, Y., He, H., Dai, N., & Du, L. (2022). Effect of altered gut microbiota on visceral hypersensitivity of postinfectious irritable bowel syndrome mice. European Journal of Gastroenterology & Hepatology, 34(12), 1220-1230. https://doi.org/10.1097/MEG.0000000000002441
Cheng F, et al. Effect of Altered Gut Microbiota On Visceral Hypersensitivity of Postinfectious Irritable Bowel Syndrome Mice. Eur J Gastroenterol Hepatol. 2022 12 1;34(12):1220-1230. PubMed PMID: 36165068.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of altered gut microbiota on visceral hypersensitivity of postinfectious irritable bowel syndrome mice. AU - Cheng,Fangli, AU - Fan,Zhenzhen, AU - Lin,Chenhong, AU - Zhu,Yubin, AU - He,Huiqin, AU - Dai,Ning, AU - Du,Lijun, Y1 - 2022/09/12/ PY - 2022/9/28/pubmed PY - 2022/11/3/medline PY - 2022/9/27/entrez SP - 1220 EP - 1230 JF - European journal of gastroenterology & hepatology JO - Eur J Gastroenterol Hepatol VL - 34 IS - 12 N2 - OBJECTIVE: Irritable bowel syndrome (IBS) is a common functional bowel disorder characterized with visceral hypersensitivity. Previous studies indicated gut microbiota alteration associated short-chain fatty acids (SCFAs) dysregulation is associated with IBS development. The aim of the study is to explore the potential role of microbiota dysbiosis mediated visceral hypersensitivity in postinfectious-IBS (PI-IBS) mouse model. METHODS: Four-week-old NIH mice were randomly allocated into four groups: control mice, PI-IBS mice, PI-IBS mice co-housing with normal mice, and PI-IBS mice were administrated with a cocktail of antibiotics. Trichinella spiralis infection established PI-IBS mouse model. Microbiota in cecal contents and feces were analyzed by 16S rDNA sequencing. SCFAs were detected by gas chromatography. 5-hydroxytryptamine (5-HT) was evaluated by ELISA, and N-methyl-D-aspartate receptors (NMDARs) were examined by western blot. Visceral sensitivity was determined by abdominal withdrawal reflex in response to colorectal distention. RESULTS: Increased SCFAs were observed in cecal contents and feces in PI-IBS mice accompanied with higher 5-HT and NMDAR subunits expressions in ileum and colon. Visceral hypersensitivity was observed in PI-IBS mice compared to control mice. When administrated with antibiotics cocktails and co-housing with normal mice, PI-IBS mice showed decreased SCFAs, 5-HT, NMDAR subunits expressions, and improved visceral hypersensitivity. CONCLUSION: Gut microbiota alteration induced increased SCFAs, 5-HT and NMDAR subunits expressions were associated with visceral hypersensitivity in PI-IBS mice. The critical role of gut microbiota in improving visceral hypersensitivity was further identified by treatment of antibiotics cocktail and co-housing. SN - 1473-5687 UR - https://www.unboundmedicine.com/medline/citation/36165068/Effect_of_altered_gut_microbiota_on_visceral_hypersensitivity_of_postinfectious_irritable_bowel_syndrome_mice_ DB - PRIME DP - Unbound Medicine ER -