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The hypoxia\u2010inducible factor\u20101\u03b1 (<jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content>\u20101\u03b1) promotes an adaptive transcriptional response to hypoxia and as such is a major regulator of immune cell survival and function. <jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content> hydroxylases are the family of oxygen\u2010sensing enzymes primarily responsible for conferring oxygen dependence upon the <jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content> pathway.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Using a mouse model of allergic contact dermatitis (<jats:styled-content style=\"fixed-case\">ACD<\/jats:styled-content>), we tested the effects of treatment with the pharmacologic hydroxylase inhibitor <jats:styled-content style=\"fixed-case\">DMOG<\/jats:styled-content>, which mimics hypoxia, on disease development.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Re\u2010exposure of sensitized mice to 2,4\u2010dinitrofluorobenzene (<jats:styled-content style=\"fixed-case\">DNFB<\/jats:styled-content>) elicited inflammation, edema, chemokine synthesis (including <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>1 and <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>5) and the recruitment of neutrophils and eosinophils. Intraperitoneal or topical application of the pharmacologic hydroxylase inhibitors dymethyloxalylglycine (<jats:styled-content style=\"fixed-case\">DMOG<\/jats:styled-content>) or <jats:styled-content style=\"fixed-case\">JNJ<\/jats:styled-content>1935 attenuated this inflammatory response. Reduced inflammation was associated with diminished recruitment of neutrophils and eosinophils but not lymphocytes. Finally, hydroxylase inhibition reduced cytokine\u2010induced chemokine production in cultured primary keratinocytes through attenuation of the <jats:styled-content style=\"fixed-case\">JNK<\/jats:styled-content> pathway.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These data demonstrate that hydroxylase inhibition attenuates the recruitment of neutrophils to inflamed skin through reduction of chemokine production and increased neutrophilic apoptosis. Thus, pharmacologic inhibition of <jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content> hydroxylases may be an effective new therapeutic approach in allergic skin inflammation.<\/jats:p><\/jats:sec>","DOI":"10.1111\/all.13655","type":"journal-article","created":{"date-parts":[[2018,11,5]],"date-time":"2018-11-05T11:52:13Z","timestamp":1541418733000},"page":"753-766","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Pharmacologic inhibition of hypoxia\u2010inducible factor (HIF)\u2010hydroxylases ameliorates allergic contact dermatitis"],"prefix":"10.1111","volume":"74","author":[{"given":"Mario C.","family":"Manresa","sequence":"first","affiliation":[{"name":"UCD Charles Institute of Dermatology School of Medicine and Medical Science University College Dublin Belfield, Dublin Ireland"},{"name":"Conway Institute of Biomedical and Biomolecular Research School of Medicine and Medical Science University 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