Calcipotriol increases hCAP18 mRNA expression but inhibits extracellular LL37 peptide production in IL-17/IL-22-stimulated normal human epidermal keratinocytes
Interleukins (IL)-17A and -22 are involved in the patho-genesis of psoriasis. Cathelicidin LL37 serves as not only antimicrobial peptide but also as autoinflammatory mediator. 1,25-Dihydroxyvitamin D3 analogues, such as calcipotriol, are used as topical treatment for psoriasis. However, the effect o...
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| Veröffentlicht in: | Acta dermato-venereologica 2014-01, Vol.94 (5), p.512-516 |
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| creator | Sakabe, Jun-ichi Umayahara, Takatsune Hiroike, Mizuho Shimauchi, Takatoshi Ito, Taisuke Tokura, Yoshiki |
| description | Interleukins (IL)-17A and -22 are involved in the patho-genesis of psoriasis. Cathelicidin LL37 serves as not only antimicrobial peptide but also as autoinflammatory mediator. 1,25-Dihydroxyvitamin D3 analogues, such as calcipotriol, are used as topical treatment for psoriasis. However, the effect of calcipotriol on the mRNA expression/production of human cathelicidin antimicrobial protein (hCAP18) and LL37 peptide by IL-17A/IL-22-stimulated keratinocytes remains controversial. To evaluate the modulatory action of calcipotriol on the production of hCAP18 and LL37, we analysed hCAP18 mRNA expression and hCAP18/LL37 peptide production in IL-17A/IL-22-stimulated cultured human keratinocytes by real-time qPCR, ELISA, western blotting, and immunocytostaining. By western blotting, hCAP18 protein was detected in keratinocytes cultured for 72 h with IL-17/IL-22. Calcipotriol increased hCAP18 mRNA expression in IL-17/IL-22-stimulated keratinocytes. However, LL37 peptide in the culture supernatants was reduced by calcipotriol. Immunostaining revealed that the overproduced LL37 resides within the cells. LL37 promotes psoriasis via interaction with extracellular DNA, but may suppress psoriasis by interfering cytosolic DNA. |
| doi_str_mv | 10.2340/00015555-1775 |
| format | Article |
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Cathelicidin LL37 serves as not only antimicrobial peptide but also as autoinflammatory mediator. 1,25-Dihydroxyvitamin D3 analogues, such as calcipotriol, are used as topical treatment for psoriasis. However, the effect of calcipotriol on the mRNA expression/production of human cathelicidin antimicrobial protein (hCAP18) and LL37 peptide by IL-17A/IL-22-stimulated keratinocytes remains controversial. To evaluate the modulatory action of calcipotriol on the production of hCAP18 and LL37, we analysed hCAP18 mRNA expression and hCAP18/LL37 peptide production in IL-17A/IL-22-stimulated cultured human keratinocytes by real-time qPCR, ELISA, western blotting, and immunocytostaining. By western blotting, hCAP18 protein was detected in keratinocytes cultured for 72 h with IL-17/IL-22. Calcipotriol increased hCAP18 mRNA expression in IL-17/IL-22-stimulated keratinocytes. However, LL37 peptide in the culture supernatants was reduced by calcipotriol. Immunostaining revealed that the overproduced LL37 resides within the cells. LL37 promotes psoriasis via interaction with extracellular DNA, but may suppress psoriasis by interfering cytosolic DNA.</description><identifier>ISSN: 0001-5555</identifier><identifier>EISSN: 1651-2057</identifier><identifier>DOI: 10.2340/00015555-1775</identifier><identifier>PMID: 24419155</identifier><language>eng</language><publisher>Sweden</publisher><subject>Antimicrobial Cationic Peptides - genetics ; Antimicrobial Cationic Peptides - metabolism ; Calcitriol - analogs & derivatives ; Calcitriol - pharmacology ; Cathelicidins - metabolism ; Cells, Cultured ; Dermatologic Agents - pharmacology ; Humans ; Interleukin-17 - pharmacology ; Interleukin-22 ; Interleukin-8 - genetics ; Interleukin-8 - metabolism ; Interleukins - pharmacology ; Keratinocytes - metabolism ; RNA, Messenger - metabolism</subject><ispartof>Acta dermato-venereologica, 2014-01, Vol.94 (5), p.512-516</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c398t-81ce9e09c0c28cb2984f64428ea2e0b985d41175eeb96d47e8f8e3c60913cab73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24419155$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sakabe, Jun-ichi</creatorcontrib><creatorcontrib>Umayahara, Takatsune</creatorcontrib><creatorcontrib>Hiroike, Mizuho</creatorcontrib><creatorcontrib>Shimauchi, Takatoshi</creatorcontrib><creatorcontrib>Ito, Taisuke</creatorcontrib><creatorcontrib>Tokura, Yoshiki</creatorcontrib><title>Calcipotriol increases hCAP18 mRNA expression but inhibits extracellular LL37 peptide production in IL-17/IL-22-stimulated normal human epidermal keratinocytes</title><title>Acta dermato-venereologica</title><addtitle>Acta Derm Venereol</addtitle><description>Interleukins (IL)-17A and -22 are involved in the patho-genesis of psoriasis. Cathelicidin LL37 serves as not only antimicrobial peptide but also as autoinflammatory mediator. 1,25-Dihydroxyvitamin D3 analogues, such as calcipotriol, are used as topical treatment for psoriasis. However, the effect of calcipotriol on the mRNA expression/production of human cathelicidin antimicrobial protein (hCAP18) and LL37 peptide by IL-17A/IL-22-stimulated keratinocytes remains controversial. To evaluate the modulatory action of calcipotriol on the production of hCAP18 and LL37, we analysed hCAP18 mRNA expression and hCAP18/LL37 peptide production in IL-17A/IL-22-stimulated cultured human keratinocytes by real-time qPCR, ELISA, western blotting, and immunocytostaining. By western blotting, hCAP18 protein was detected in keratinocytes cultured for 72 h with IL-17/IL-22. Calcipotriol increased hCAP18 mRNA expression in IL-17/IL-22-stimulated keratinocytes. However, LL37 peptide in the culture supernatants was reduced by calcipotriol. Immunostaining revealed that the overproduced LL37 resides within the cells. LL37 promotes psoriasis via interaction with extracellular DNA, but may suppress psoriasis by interfering cytosolic DNA.</description><subject>Antimicrobial Cationic Peptides - genetics</subject><subject>Antimicrobial Cationic Peptides - metabolism</subject><subject>Calcitriol - analogs & derivatives</subject><subject>Calcitriol - pharmacology</subject><subject>Cathelicidins - metabolism</subject><subject>Cells, Cultured</subject><subject>Dermatologic Agents - pharmacology</subject><subject>Humans</subject><subject>Interleukin-17 - pharmacology</subject><subject>Interleukin-22</subject><subject>Interleukin-8 - genetics</subject><subject>Interleukin-8 - metabolism</subject><subject>Interleukins - pharmacology</subject><subject>Keratinocytes - metabolism</subject><subject>RNA, Messenger - metabolism</subject><issn>0001-5555</issn><issn>1651-2057</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kU1PxCAQhonRuOvq0avh6AUXKG3pcbPxY5NGjdFzQ-k0i_ZLoIn7a_yrUt2Vw5BhnneYyYvQJaM3PBJ0SSllcTiEpWl8hOYsiRnhNE6P0Xyqkak4Q2fOvYeUx0yeohkXgmVBNkffa9VoM_Temr7BptMWlAOHt-vVM5O4fXlcYfgaLDhn-g6Xow_Q1pTGu_DurdLQNGOjLM7zKMUDDN5UgAfbV6P2k8R0eJOH6ZYhck6cN23gPVS4622rGrwdW9VhGILuN_8Aq7zper3z4M7RSa0aBxf7e4He7m5f1w8kf7rfrFc50VEmPZFMQwY001RzqUueSVEnQnAJigMtMxlXgrE0BiizpBIpyFpCpBOasUirMo0W6Pqvb5j8cwTni9a4aTfVQT-6gsVJ-IiKiAaU_KHa9s5ZqIvBmlbZXcFoMXlSHDwpJk8Cf7VvPZYtVP_0wYToBz9mh_E</recordid><startdate>20140101</startdate><enddate>20140101</enddate><creator>Sakabe, Jun-ichi</creator><creator>Umayahara, Takatsune</creator><creator>Hiroike, Mizuho</creator><creator>Shimauchi, Takatoshi</creator><creator>Ito, Taisuke</creator><creator>Tokura, Yoshiki</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20140101</creationdate><title>Calcipotriol increases hCAP18 mRNA expression but inhibits extracellular LL37 peptide production in IL-17/IL-22-stimulated normal human epidermal keratinocytes</title><author>Sakabe, Jun-ichi ; Umayahara, Takatsune ; Hiroike, Mizuho ; Shimauchi, Takatoshi ; Ito, Taisuke ; Tokura, Yoshiki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c398t-81ce9e09c0c28cb2984f64428ea2e0b985d41175eeb96d47e8f8e3c60913cab73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Antimicrobial Cationic Peptides - genetics</topic><topic>Antimicrobial Cationic Peptides - metabolism</topic><topic>Calcitriol - analogs & derivatives</topic><topic>Calcitriol - pharmacology</topic><topic>Cathelicidins - metabolism</topic><topic>Cells, Cultured</topic><topic>Dermatologic Agents - pharmacology</topic><topic>Humans</topic><topic>Interleukin-17 - pharmacology</topic><topic>Interleukin-22</topic><topic>Interleukin-8 - genetics</topic><topic>Interleukin-8 - metabolism</topic><topic>Interleukins - pharmacology</topic><topic>Keratinocytes - metabolism</topic><topic>RNA, Messenger - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sakabe, Jun-ichi</creatorcontrib><creatorcontrib>Umayahara, Takatsune</creatorcontrib><creatorcontrib>Hiroike, Mizuho</creatorcontrib><creatorcontrib>Shimauchi, Takatoshi</creatorcontrib><creatorcontrib>Ito, Taisuke</creatorcontrib><creatorcontrib>Tokura, Yoshiki</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Acta dermato-venereologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sakabe, Jun-ichi</au><au>Umayahara, Takatsune</au><au>Hiroike, Mizuho</au><au>Shimauchi, Takatoshi</au><au>Ito, Taisuke</au><au>Tokura, Yoshiki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Calcipotriol increases hCAP18 mRNA expression but inhibits extracellular LL37 peptide production in IL-17/IL-22-stimulated normal human epidermal keratinocytes</atitle><jtitle>Acta dermato-venereologica</jtitle><addtitle>Acta Derm Venereol</addtitle><date>2014-01-01</date><risdate>2014</risdate><volume>94</volume><issue>5</issue><spage>512</spage><epage>516</epage><pages>512-516</pages><issn>0001-5555</issn><eissn>1651-2057</eissn><abstract>Interleukins (IL)-17A and -22 are involved in the patho-genesis of psoriasis. Cathelicidin LL37 serves as not only antimicrobial peptide but also as autoinflammatory mediator. 1,25-Dihydroxyvitamin D3 analogues, such as calcipotriol, are used as topical treatment for psoriasis. However, the effect of calcipotriol on the mRNA expression/production of human cathelicidin antimicrobial protein (hCAP18) and LL37 peptide by IL-17A/IL-22-stimulated keratinocytes remains controversial. To evaluate the modulatory action of calcipotriol on the production of hCAP18 and LL37, we analysed hCAP18 mRNA expression and hCAP18/LL37 peptide production in IL-17A/IL-22-stimulated cultured human keratinocytes by real-time qPCR, ELISA, western blotting, and immunocytostaining. By western blotting, hCAP18 protein was detected in keratinocytes cultured for 72 h with IL-17/IL-22. Calcipotriol increased hCAP18 mRNA expression in IL-17/IL-22-stimulated keratinocytes. However, LL37 peptide in the culture supernatants was reduced by calcipotriol. Immunostaining revealed that the overproduced LL37 resides within the cells. LL37 promotes psoriasis via interaction with extracellular DNA, but may suppress psoriasis by interfering cytosolic DNA.</abstract><cop>Sweden</cop><pmid>24419155</pmid><doi>10.2340/00015555-1775</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antimicrobial Cationic Peptides - genetics Antimicrobial Cationic Peptides - metabolism Calcitriol - analogs & derivatives Calcitriol - pharmacology Cathelicidins - metabolism Cells, Cultured Dermatologic Agents - pharmacology Humans Interleukin-17 - pharmacology Interleukin-22 Interleukin-8 - genetics Interleukin-8 - metabolism Interleukins - pharmacology Keratinocytes - metabolism RNA, Messenger - metabolism |
| title | Calcipotriol increases hCAP18 mRNA expression but inhibits extracellular LL37 peptide production in IL-17/IL-22-stimulated normal human epidermal keratinocytes |
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