{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T15:17:06Z","timestamp":1778253426494,"version":"3.51.4"},"reference-count":33,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2012,11,22]],"date-time":"2012-11-22T00:00:00Z","timestamp":1353542400000},"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":[[2012,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Ultraviolet B (<jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>) radiation induces inflammation in the skin specifically at the site of exposure. We unexpectedly found that<jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\u2010induced inflammation was not induced in gp91phox\u2010depleted mice. To test whether gp91phox is directly involved in<jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\u2010induced inflammation, neutrophil\u2010 and hyaluronic acid\u2013depleted mice were also irradiated and examined for their response. Hyaluronic acid\u2013depleted mice showed strongly inhibited<jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\u2010induced inflammation, but the neutrophil\u2010depleted mice did not exhibit any suppressed<jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\u2010induced inflammation. To elucidate the pathway by which<jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>irradiation induced inflammation, we examined the expression of nucleotide\u2010binding domain, leucine\u2010rich\u2010containing family, pyrin domain\u2010containing\u20103 (<jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>3) and caspase\u20101 in the mouse skin. An increase in the expression of<jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>3 and caspase\u20101 was seen following the<jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>irradiation of C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>mice; however, the<jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\u2010irradiated gp91phox\u2010knockout (gp91phox<jats:sup>\u2212\/\u2212<\/jats:sup>) mice did not have this increase in expression. Furthermore, the plasma<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 level increased after the<jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>irradiation in C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>mice, but there was no change in the gp91phox<jats:sup>\u2212\/\u2212<\/jats:sup>mice. These results clearly indicate that nicotinamide adenine dinucleotide phosphate oxidase is activated by gp91phox, which is expressed on the surface in response to the increased expression of hyaluronic acid induced by<jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>irradiation, and as result, the generation of reactive oxygen species (<jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>) increases. This<jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>activate<jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>3, and<jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>3 leads to the production of caspase\u20101, which subsequently increases<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2, thereby finally inducing inflammation. It is thought that this system may play an important role in the damage and ageing of skin, and further studies are necessary to confirm these finding.<\/jats:p>","DOI":"10.1111\/exd.12032","type":"journal-article","created":{"date-parts":[[2012,9,24]],"date-time":"2012-09-24T01:48:04Z","timestamp":1348451284000},"page":"911-914","source":"Crossref","is-referenced-by-count":33,"title":["Intercellular pathway through hyaluronic acid in<scp>UVB<\/scp>\u2010induced inflammation"],"prefix":"10.1111","volume":"21","author":[{"given":"Keiichi","family":"Hiramoto","sequence":"first","affiliation":[{"name":"Department of Dermatology Osaka City University Graduate School of Medicine Osaka Japan"},{"name":"Brain Science Institute Osaka City University Graduate School of Medicine Osaka Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiromi","family":"Kobayashi","sequence":"additional","affiliation":[{"name":"Department of Dermatology Osaka City University Graduate School of Medicine Osaka Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yurika","family":"Yamate","sequence":"additional","affiliation":[{"name":"Department of Dermatology Osaka City University Graduate School of Medicine Osaka Japan"},{"name":"Brain Science Institute Osaka City University Graduate School of Medicine Osaka Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masamitsu","family":"Ishii","sequence":"additional","affiliation":[{"name":"Department of Dermatology Osaka City University Graduate School of Medicine Osaka Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eisuke F.","family":"Sato","sequence":"additional","affiliation":[{"name":"Brain Science Institute Osaka City University Graduate School of Medicine Osaka 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