Transitional changes in gastrointestinal transit and rectal sensitivity from active to recovery of inflammation in a rodent model of colitis

Abstract Patients with ulcerative colitis are typically suspected of an inflammatory flare based on suggestive symptoms of inflammation. The aim of this study was to evaluate the impact of inflammation on colonic motility and rectal sensitivity from active to recovery of inflammation. Male rats were...

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Main Authors: Yan Chen, Yu Guo, Payam Gharibani, Jie Chen, Florin M. Selaru, Jiande D. Z. Chen
Format: Article
Language:English
Published: Nature Publishing Group 2021-04-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-021-87814-7
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spelling doaj-bd1bd660241f45fba680504e583ecb1a2021-04-18T11:36:04ZengNature Publishing GroupScientific Reports2045-23222021-04-011111910.1038/s41598-021-87814-7Transitional changes in gastrointestinal transit and rectal sensitivity from active to recovery of inflammation in a rodent model of colitisYan Chen0Yu Guo1Payam Gharibani2Jie Chen3Florin M. Selaru4Jiande D. Z. Chen5Division of Gastroenterology and Hepatology, Johns Hopkins University School of MedicineDivision of Gastroenterology and Hepatology, Johns Hopkins University School of MedicineDivision of Gastroenterology and Hepatology, Johns Hopkins University School of MedicineDivision of Gastroenterology and Hepatology, Johns Hopkins University School of MedicineDivision of Gastroenterology and Hepatology, Johns Hopkins University School of MedicineDivision of Gastroenterology and Hepatology, Johns Hopkins University School of MedicineAbstract Patients with ulcerative colitis are typically suspected of an inflammatory flare based on suggestive symptoms of inflammation. The aim of this study was to evaluate the impact of inflammation on colonic motility and rectal sensitivity from active to recovery of inflammation. Male rats were given drinking water with 5% dextran sulfate sodium for 7 days. Inflammation, intestinal motor and sensory functions were investigated weekly for 6 weeks. (1) The disease activity index score, fecal calprotectin and tumor necrosis factor alpha were increased from Day 0 to Day 7 (active inflammation) and then decreased gradually until recovery. (2) Distal colon transit was accelerated on Day 7, and then remained unchanged. Whole gut transit was delayed on Day 7 but accelerated from Day 14 to Day 42. (3) Rectal compliance was unaffected from Day 0 to Day 7, but decreased afterwards. (4) Rectal hypersensitivity was noted on Day 7 and persistent. (5) Plasma acetylcholine was decreased on Day 7 but increased from Day 14 to Day 42. Nerve growth factor was increased from Day 7 to Day 42. DSS-induced inflammation leads to visceral hypersensitivity that is sustained until the resolution of inflammation, probably mediated by NGF. Rectal compliance is reduced one week after the DSS-induced inflammation and the reduction is sustained until the resolution of inflammation. Gastrointestinal transit is also altered during and after active colonic inflammation.https://doi.org/10.1038/s41598-021-87814-7
collection DOAJ
language English
format Article
sources DOAJ
author Yan Chen
Yu Guo
Payam Gharibani
Jie Chen
Florin M. Selaru
Jiande D. Z. Chen
spellingShingle Yan Chen
Yu Guo
Payam Gharibani
Jie Chen
Florin M. Selaru
Jiande D. Z. Chen
Transitional changes in gastrointestinal transit and rectal sensitivity from active to recovery of inflammation in a rodent model of colitis
Scientific Reports
author_facet Yan Chen
Yu Guo
Payam Gharibani
Jie Chen
Florin M. Selaru
Jiande D. Z. Chen
author_sort Yan Chen
title Transitional changes in gastrointestinal transit and rectal sensitivity from active to recovery of inflammation in a rodent model of colitis
title_short Transitional changes in gastrointestinal transit and rectal sensitivity from active to recovery of inflammation in a rodent model of colitis
title_full Transitional changes in gastrointestinal transit and rectal sensitivity from active to recovery of inflammation in a rodent model of colitis
title_fullStr Transitional changes in gastrointestinal transit and rectal sensitivity from active to recovery of inflammation in a rodent model of colitis
title_full_unstemmed Transitional changes in gastrointestinal transit and rectal sensitivity from active to recovery of inflammation in a rodent model of colitis
title_sort transitional changes in gastrointestinal transit and rectal sensitivity from active to recovery of inflammation in a rodent model of colitis
publisher Nature Publishing Group
series Scientific Reports
issn 2045-2322
publishDate 2021-04-01
description Abstract Patients with ulcerative colitis are typically suspected of an inflammatory flare based on suggestive symptoms of inflammation. The aim of this study was to evaluate the impact of inflammation on colonic motility and rectal sensitivity from active to recovery of inflammation. Male rats were given drinking water with 5% dextran sulfate sodium for 7 days. Inflammation, intestinal motor and sensory functions were investigated weekly for 6 weeks. (1) The disease activity index score, fecal calprotectin and tumor necrosis factor alpha were increased from Day 0 to Day 7 (active inflammation) and then decreased gradually until recovery. (2) Distal colon transit was accelerated on Day 7, and then remained unchanged. Whole gut transit was delayed on Day 7 but accelerated from Day 14 to Day 42. (3) Rectal compliance was unaffected from Day 0 to Day 7, but decreased afterwards. (4) Rectal hypersensitivity was noted on Day 7 and persistent. (5) Plasma acetylcholine was decreased on Day 7 but increased from Day 14 to Day 42. Nerve growth factor was increased from Day 7 to Day 42. DSS-induced inflammation leads to visceral hypersensitivity that is sustained until the resolution of inflammation, probably mediated by NGF. Rectal compliance is reduced one week after the DSS-induced inflammation and the reduction is sustained until the resolution of inflammation. Gastrointestinal transit is also altered during and after active colonic inflammation.
url https://doi.org/10.1038/s41598-021-87814-7
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