https://ogma.newcastle.edu.au/vital/access/ /manager/Index en-au 5 Systematic Review on the Influence of Tissue Oxygenation on Gut Microbiota and Anastomotic Healing https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42656 Wed 31 Aug 2022 13:02:16 AEST ]]> Chronic cigarette smoke exposure induces systemic hypoxia that drives intestinal dysfunction https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38040 Wed 28 Jul 2021 10:17:50 AEST ]]> PAI-1 augments mucosal damage in colitis https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47717 Wed 25 Jan 2023 13:01:40 AEDT ]]> Platelet activating factor receptor regulates colitis-induced pulmonary inflammation through the NLRP3 inflammasome https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:48579 Tue 21 Mar 2023 17:43:58 AEDT ]]> The bile acids, deoxycholic acid and ursodeoxycholic acid, regulate colonic epithelial wound healing https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35651 84 cell monolayers grown on transparent, permeable supports was assessed over 48 h with or without bile acids. Cell migration was measured in Boyden chambers. mRNA and protein expression were measured by RT-PCR and Western blotting. DCA (50-150 μM) significantly inhibited wound closure in cultured epithelial monolayers and attenuated cell migration in Boyden chamber assays. DCA also induced nuclear accumulation of the farnesoid X receptor (FXR), whereas an FXR agonist, GW4064 (10 µM), inhibited wound closure. Both DCA and GW4064 attenuated the expression of CFTR Cl⁻ channels, whereas inhibition of CFTR activity with either CFTR-inh-172 (10 μM) or GlyH-101 (25 µM) also prevented wound healing. Promoter/reporter assays revealed that FXR-induced downregulation of CFTR is mediated at the transcriptional level. In contrast, UDCA (50-150 µM) enhanced wound healing in vitro and prevented the effects of DCA. Finally, DCA inhibited and UDCA promoted mucosal healing in an in vivo mouse model. In conclusion, these studies suggest bile acids are important regulators of epithelial wound healing and are therefore good targets for development of new drugs to modulate intestinal barrier function in disease treatment. New & Noteworthy: The secondary bile acid, deoxycholic acid, inhibits colonic epithelial wound healing, an effect which appears to be mediated by activation of the nuclear bile acid receptor, FXR, with subsequent downregulation of CFTR expression and activity. In contrast, ursodeoxycholic acid promotes wound healing, suggesting it may provide an alternative approach to prevent the losses of barrier function that are associated with mucosal inflammation in IBD patients.]]> Tue 01 Oct 2019 13:39:00 AEST ]]> IL-6 drives neutrophil-mediated pulmonary inflammation associated with bacteremia in murine models of colitis https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34597 Thu 13 Jan 2022 10:31:31 AEDT ]]> Defects in NLRP6, autophagy and goblet cell homeostasis are associated with reduced duodenal CRH receptor 2 expression in patients with functional dyspepsia https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49117 Thu 02 May 2024 12:18:23 AEST ]]> Oral delivery of prolyl hydroxylase inhibitor: AKB-4924 promotes localized mucosal healing in a mouse model of colitis https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27125 Fri 25 Sep 2020 11:41:05 AEST ]]> Platelet activating factor receptor acts to limit colitis-induced liver inflammation https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41982 Fri 19 Apr 2024 11:58:15 AEST ]]> Pharmacological HIF-1 stabilization promotes intestinal epithelial healing through regulation of α-integrin expression and function https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49107 Fri 05 May 2023 11:32:08 AEST ]]>