{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T19:27:31Z","timestamp":1770233251968,"version":"3.49.0"},"reference-count":41,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2015,8,18]],"date-time":"2015-08-18T00:00:00Z","timestamp":1439856000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2015,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Dry skin has been clinically associated with visceral diseases, including liver disease, as well as for our previously reported small intestinal injury mouse model, which have abnormalities in skin barrier function. To clarify this disease\u2010induced skin disruption, we used a dextran sulphate sodium (<jats:styled-content style=\"fixed-case\">DSS<\/jats:styled-content>)\u2010induced colitis mouse model. Following treatment with <jats:styled-content style=\"fixed-case\">DSS<\/jats:styled-content>, damage to the colon and skin was monitored using histological and protein analysis methods as well as the detection of inflammatory mediators in the plasma. Notably, transepidermal water loss was higher, and skin hydration was lower in <jats:styled-content style=\"fixed-case\">DSS<\/jats:styled-content>\u2010treated mice compared to controls. Tumor necrosis factor\u2010alpha (<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010<jats:italic>\u03b1<\/jats:italic>), interleukin 6 and <jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/exd12775-math-0002.png\" xlink:title=\"urn:x-wiley:09066705:media:exd12775:exd12775-math-0002\"\/> levels were also upregulated in the plasma, and a decrease in body weight and colon length was observed in <jats:styled-content style=\"fixed-case\">DSS<\/jats:styled-content>\u2010treated mice. However, when administered <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010<jats:italic>\u03b1<\/jats:italic> antibody or an <jats:styled-content style=\"fixed-case\">iNOS<\/jats:styled-content> inhibitor, no change in skin condition was observed, indicating that another signalling mechanism is utilized. Interestingly, the number of tryptase\u2010expressing mast cells, known for their role in immune function via cholinergic signal transduction, was elevated. To evaluate the function of cholinergic signalling in this context, atropine (a muscarinic cholinoceptor antagonist) or hexamethonium (a nicotinic cholinergic ganglion\u2010blocking agent) was administered to <jats:styled-content style=\"fixed-case\">DSS<\/jats:styled-content>\u2010treated mice. Our data indicate that muscarinic acetylcholine receptors (m<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>s) are the primary receptors functioning in colon\u2010to\u2010skin signal transduction, as <jats:styled-content style=\"fixed-case\">DSS<\/jats:styled-content>\u2010induced skin disruption was suppressed by atropine. Thus, skin disruption is likely associated with <jats:styled-content style=\"fixed-case\">DSS<\/jats:styled-content>\u2010induced colitis, and the activation of mast cells via m<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>s is critical to this association.<\/jats:p>","DOI":"10.1111\/exd.12775","type":"journal-article","created":{"date-parts":[[2015,5,27]],"date-time":"2015-05-27T14:20:00Z","timestamp":1432736400000},"page":"779-784","source":"Crossref","is-referenced-by-count":27,"title":["Impairment of skin barrier function via cholinergic signal transduction in a dextran sulphate sodium\u2010induced colitis mouse model"],"prefix":"10.1111","volume":"24","author":[{"given":"Satoshi","family":"Yokoyama","sequence":"first","affiliation":[{"name":"Faculty of Pharmaceutical Sciences Suzuka University of Medical Science Mie 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