Vanilloid receptor-1 containing primary sensory neurones mediate dextran sulphate sodium induced colitis in rats

Kihara, Norio; Fuente, Sebastián G. de la; Fujino, Kazunori; Takahashi, Tatsuhiko; Pappas, Theodore N.; Mantyh, Christopher R.

doi:10.1136/gut.52.5.713

Cited by 232 publications

(195 citation statements)

References 33 publications

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“…In agreement with published data [39][40][41][42][43][44] , the DAI increased gradually over the time of DSS administration, reaching a maximum of 3.11 ± 0.05 on the last day of DSS administration (day 7), and subsequently decreased to 1.55 ± 0.17 at the 4 th day after DSS cessation. The full DAI time course is shown in Fig.1.…”

Section: Resultssupporting

confidence: 79%

On the dynamics of nitrite, nitrate and other biomarkers of nitric oxide production in inflammatory bowel disease

et al. 2010

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Section: Resultssupporting

confidence: 79%

On the dynamics of nitrite, nitrate and other biomarkers of nitric oxide production in inflammatory bowel disease

et al. 2010

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“…The disease activity index (DAI) has been commonly used to evaluate the grade and extent of acute colitis 18 . The DAI score ranges from 0 to 4, representing the sum of scores for weight loss, stool consistency and rectal bleeding, divided by three.…”

Section: Myh9 Monoallelic Deletion Ameliorates Dss-induced Colitismentioning

confidence: 99%

The non-muscle-myosin-II heavy chain Myh9 mediates colitis-induced epithelium injury by restricting Lgr5+ stem cells

Zhao

et al. 2015

Nat Commun

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Lgr5 þ stem cells are crucial to gut epithelium homeostasis, and therapies targeting these cells hold promise for treatment of gastrointestinal diseases. Here we report that the non-muscle-myosin-II (NMII) heavy chain Myh9 accumulates at epithelial injury sites in mice distal colon treated with dextran sulphate sodium (DSS). Gut-epithelium-specific Myh9 monoallelic deletion alleviates DSS-induced colonic crypt damage and acute colitis. Consistently, the NMII inhibitor blebbistatin can improve the survival of Lgr5 þ stem cells and the growth of Lgr5 organoids. Mechanistically, inhibition of NMII by blebbistatin or Myh9 monoallelic deletion activates Akt through Rac1 and PAK1, which is essential for the survival and pluripotency of Lgr5 þ cells. These results establish a critical role of the Myh9-Rac1-PAK1-Akt pathway in the maintenance of Lgr5 þ stem cells. As blebbistatin can mitigate DSS-induced colitis and preserve Lgr5 þ colonic stem cells in vivo, our findings provide a potential therapeutic intervention of gastrointestinal epithelium injury and degenerative diseases.

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“…These parameters were each assigned a score and utilized to calculate an average daily disease activity index (DAI) score for each mouse as previously described [22] .…”

Section: Evaluation Of Daimentioning

confidence: 99%

“…Acute colitis was induced in mice by replacing normal drinking water with distilled water containing 5% (w/v) DSS and allowing them to drink freely for 7 days [22] . The mice in the DSS group and the three balsalazine groups all drank 5% DSS, and the mice in the control group received regular distilled water.…”

Section: Induction Of Colitismentioning

confidence: 99%

Balsalazine decreases intestinal mucosal permeability of dextran sulfate sodium-induced colitis in mice

Liu

Qiao

et al. 2009

Acta Pharmacol Sin

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Aim:To investigate the effect of balsalazine treatment on intestinal mucosal permeability in dextran sulfate sodium (DSS)-induced colitis and to determine the mechanism of the balsalazine-induced changes. Methods: Experimental colitis was induced in C57BL/6J mice by the administration of 5% DSS. Balsalazine was administered intragastrically at doses of 42, 141, and 423 mg/kg. The disease activity index (DAI) score was evaluated and colon tissue was collected for the assessment of histological changes. The amount of malondialdehyde (MDA) in the colon was determined, along with the activity of myeloperoxidase (MPO), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Mucosa from the small intestine was collected to determine the levels of tumor necrosis factor (TNF)-α and interferon (IFN)-γ. The mucosa was ultrastructurally examined with transmission electron microscopy and intestinal permeability was assayed using Evans blue. Results: Balsalazine was found to reduce the DAI score and the histological index (HI) score, decrease the MDA content and the activity of MPO, and increase the activity of SOD and GSH-Px in colitis mice. At the same time, balsalazine ameliorated microvillus and tight junction structure, resulting in a decrease in the amount of Evans blue permeating into the intestinal wall and the levels of TNF-α and IFN-γ in colitis mice. Conclusion: In colitis mice, the anti-colitis effect of balsalazine results in a decrease in intestinal mucosal permeability. The mechanism of this effect is partly associated with balsalazine's antioxidative and anti-inflammatory effects.

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Vanilloid receptor-1 containing primary sensory neurones mediate dextran sulphate sodium induced colitis in rats

Abstract: Neonatal capsaicinisation and local administration of CPZ prevents intestinal inflammation in a well established model of colitis indicating that primary sensory neurones possessing VR-1 receptors are required in the propagation of colonic inflammation.

Cited by 232 publications

References 33 publications

On the dynamics of nitrite, nitrate and other biomarkers of nitric oxide production in inflammatory bowel disease

On the dynamics of nitrite, nitrate and other biomarkers of nitric oxide production in inflammatory bowel disease

The non-muscle-myosin-II heavy chain Myh9 mediates colitis-induced epithelium injury by restricting Lgr5+ stem cells

Balsalazine decreases intestinal mucosal permeability of dextran sulfate sodium-induced colitis in mice

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