IL-1α Stimulation Restores Epidermal Permeability and Antimicrobial Barriers Compromised by Topical Tacrolimus
In a previous study, we showed that barrier recovery was delayed after acute barrier disruption in the skin treated with topical calcineurin inhibitors. Tacrolimus decreases lipid synthesis and the expressions of antimicrobial peptide (AMP) and IL-1α in the epidermis. IL-1α is an important cytokine...
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| Veröffentlicht in: | Journal of investigative dermatology 2011-03, Vol.131 (3), p.698-705 |
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| creator | Jung, Ye-Jin Jung, Minyoung Kim, Minjeong Hong, Seung-Phil Choi, Eung Ho |
| description | In a previous study, we showed that barrier recovery was delayed after acute barrier disruption in the skin treated with topical calcineurin inhibitors. Tacrolimus decreases lipid synthesis and the expressions of antimicrobial peptide (AMP) and IL-1α in the epidermis. IL-1α is an important cytokine for improving barrier function, lamellar body (LB) production, and lipid synthesis in keratinocytes (KCs). We aimed to evaluate whether IL-1α stimulation could restore the barrier dysfunction observed in tacrolimus-treated skin. Topical imiquimod, an IL-1α inducer, restored the epidermal permeability barrier recovery that had been inhibited by tacrolimus treatment in human (n=15) and murine (n=10) skins, and improved stratum corneum integrity by restoring corneodosmosomes in murine skin (n=6). Imiquimod co-applied on the epidermis resulted in an increase in the production of LB and three major lipid synthesis-related enzymes, and in the expressions of mBD3, CRAMP, and IL-1α (n=5). Furthermore, intracutaneous injection of IL-1α restored permeability barrier recovery (n=6). In IL-1 type 1 receptor knockout mice, topical imiquimod was unable to restore permeability barrier recovery after tacrolimus treatment (n=21). In conclusion, IL-1α stimulation induced positive effects on epidermal permeability and antimicrobial barrier functions in tacrolimus-treated skin. These positive effects were mediated by an increase in epidermal lipid synthesis, LB production, and AMP expression.
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| doi_str_mv | 10.1038/jid.2010.344 |
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JID JOURNAL CLUB ARTICLE: For questions, answers, and open discussion about this article, please go to http://www.nature.com/jid/journalclub</description><identifier>ISSN: 0022-202X</identifier><identifier>EISSN: 1523-1747</identifier><identifier>DOI: 10.1038/jid.2010.344</identifier><identifier>PMID: 21107352</identifier><identifier>CODEN: JIDEAE</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Administration, Topical ; Adult ; Aminoquinolines - administration & dosage ; Aminoquinolines - pharmacology ; Animals ; Antimicrobial Cationic Peptides ; beta-Defensins - metabolism ; Biological and medical sciences ; Cathelicidins - metabolism ; Cell Membrane - drug effects ; Cell Membrane - microbiology ; Cell Membrane Permeability - drug effects ; Cell Membrane Permeability - physiology ; Dermatology ; Desmosomes - drug effects ; Desmosomes - physiology ; Epidermal Cells ; Epidermis - drug effects ; Epidermis - metabolism ; Female ; Humans ; Imiquimod ; Immunosuppressive Agents - administration & dosage ; Immunosuppressive Agents - pharmacology ; Interleukin-1alpha - agonists ; Interleukin-1alpha - metabolism ; Interleukin-1alpha - pharmacology ; Lipid Metabolism - drug effects ; Male ; Medical sciences ; Mice ; Mice, Hairless ; Mice, Knockout ; Middle Aged ; Models, Animal ; Receptors, Interleukin-1 - genetics ; Receptors, Interleukin-1 - metabolism ; Tacrolimus - administration & dosage ; Tacrolimus - pharmacology</subject><ispartof>Journal of investigative dermatology, 2011-03, Vol.131 (3), p.698-705</ispartof><rights>2011 The Society for Investigative Dermatology, Inc</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-c792688f060adb2c837f99324a608b214edc8bb852c04a0885968692b2428fa23</citedby><cites>FETCH-LOGICAL-c405t-c792688f060adb2c837f99324a608b214edc8bb852c04a0885968692b2428fa23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24038171$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21107352$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jung, Ye-Jin</creatorcontrib><creatorcontrib>Jung, Minyoung</creatorcontrib><creatorcontrib>Kim, Minjeong</creatorcontrib><creatorcontrib>Hong, Seung-Phil</creatorcontrib><creatorcontrib>Choi, Eung Ho</creatorcontrib><title>IL-1α Stimulation Restores Epidermal Permeability and Antimicrobial Barriers Compromised by Topical Tacrolimus</title><title>Journal of investigative dermatology</title><addtitle>J Invest Dermatol</addtitle><description>In a previous study, we showed that barrier recovery was delayed after acute barrier disruption in the skin treated with topical calcineurin inhibitors. Tacrolimus decreases lipid synthesis and the expressions of antimicrobial peptide (AMP) and IL-1α in the epidermis. IL-1α is an important cytokine for improving barrier function, lamellar body (LB) production, and lipid synthesis in keratinocytes (KCs). We aimed to evaluate whether IL-1α stimulation could restore the barrier dysfunction observed in tacrolimus-treated skin. Topical imiquimod, an IL-1α inducer, restored the epidermal permeability barrier recovery that had been inhibited by tacrolimus treatment in human (n=15) and murine (n=10) skins, and improved stratum corneum integrity by restoring corneodosmosomes in murine skin (n=6). Imiquimod co-applied on the epidermis resulted in an increase in the production of LB and three major lipid synthesis-related enzymes, and in the expressions of mBD3, CRAMP, and IL-1α (n=5). Furthermore, intracutaneous injection of IL-1α restored permeability barrier recovery (n=6). In IL-1 type 1 receptor knockout mice, topical imiquimod was unable to restore permeability barrier recovery after tacrolimus treatment (n=21). In conclusion, IL-1α stimulation induced positive effects on epidermal permeability and antimicrobial barrier functions in tacrolimus-treated skin. These positive effects were mediated by an increase in epidermal lipid synthesis, LB production, and AMP expression.
JID JOURNAL CLUB ARTICLE: For questions, answers, and open discussion about this article, please go to http://www.nature.com/jid/journalclub</description><subject>Administration, Topical</subject><subject>Adult</subject><subject>Aminoquinolines - administration & dosage</subject><subject>Aminoquinolines - pharmacology</subject><subject>Animals</subject><subject>Antimicrobial Cationic Peptides</subject><subject>beta-Defensins - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cathelicidins - metabolism</subject><subject>Cell Membrane - drug effects</subject><subject>Cell Membrane - microbiology</subject><subject>Cell Membrane Permeability - drug effects</subject><subject>Cell Membrane Permeability - physiology</subject><subject>Dermatology</subject><subject>Desmosomes - drug effects</subject><subject>Desmosomes - physiology</subject><subject>Epidermal Cells</subject><subject>Epidermis - drug effects</subject><subject>Epidermis - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Imiquimod</subject><subject>Immunosuppressive Agents - administration & dosage</subject><subject>Immunosuppressive Agents - pharmacology</subject><subject>Interleukin-1alpha - agonists</subject><subject>Interleukin-1alpha - metabolism</subject><subject>Interleukin-1alpha - pharmacology</subject><subject>Lipid Metabolism - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Hairless</subject><subject>Mice, Knockout</subject><subject>Middle Aged</subject><subject>Models, Animal</subject><subject>Receptors, Interleukin-1 - genetics</subject><subject>Receptors, Interleukin-1 - metabolism</subject><subject>Tacrolimus - administration & dosage</subject><subject>Tacrolimus - pharmacology</subject><issn>0022-202X</issn><issn>1523-1747</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkM9O3DAQhy1UBMuWG2fkS8WFUHviJM4RVkCRVmrVbqXeLP-LZJTEi51F2sfqi_BMzGq37aWnkTXfjH_zEXLB2Q1npfz8HNwNMHyVQhyRGa-gLHgjmg9kxhhAAQx-nZKznJ8Z47Wo5Ak5Bc5ZU1YwI_FpWfC33_THFIZNr6cQR_rd5ykmn-n9OjifBt3Tb1i8NqEP05bq0dHbEQeCTdEEbN_plIJPmS7isE5xCNk7arZ0FdfBYn-lkezxh_yRHHe6z_78UOfk58P9avGlWH59fFrcLgsrWDUVtmmhlrJjNdPOgJVl07VtCULXTBrgwjsrjZEVWCY0k7Jqa1m3YECA7DSUc3K134txXjZ4kMJQ1ve9Hn3cZCUrLpoK6hLJ6z2JEXNOvlPrFAadtooztTOs0LDaGVZoGPHLw-KNGbz7C_9RisCnA6Az3t4lPdqQ_3ECV_KGI1fvOY8aXtGeyjb40XoXkreTcjH8P8E7vQ6W9Q</recordid><startdate>20110301</startdate><enddate>20110301</enddate><creator>Jung, Ye-Jin</creator><creator>Jung, Minyoung</creator><creator>Kim, Minjeong</creator><creator>Hong, Seung-Phil</creator><creator>Choi, Eung Ho</creator><general>Elsevier Inc</general><general>Nature Publishing Group</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><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>20110301</creationdate><title>IL-1α Stimulation Restores Epidermal Permeability and Antimicrobial Barriers Compromised by Topical Tacrolimus</title><author>Jung, Ye-Jin ; Jung, Minyoung ; Kim, Minjeong ; Hong, Seung-Phil ; Choi, Eung Ho</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-c792688f060adb2c837f99324a608b214edc8bb852c04a0885968692b2428fa23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Administration, Topical</topic><topic>Adult</topic><topic>Aminoquinolines - administration & dosage</topic><topic>Aminoquinolines - pharmacology</topic><topic>Animals</topic><topic>Antimicrobial Cationic Peptides</topic><topic>beta-Defensins - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cathelicidins - metabolism</topic><topic>Cell Membrane - drug effects</topic><topic>Cell Membrane - microbiology</topic><topic>Cell Membrane Permeability - drug effects</topic><topic>Cell Membrane Permeability - physiology</topic><topic>Dermatology</topic><topic>Desmosomes - drug effects</topic><topic>Desmosomes - physiology</topic><topic>Epidermal Cells</topic><topic>Epidermis - drug effects</topic><topic>Epidermis - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>Imiquimod</topic><topic>Immunosuppressive Agents - administration & dosage</topic><topic>Immunosuppressive Agents - pharmacology</topic><topic>Interleukin-1alpha - agonists</topic><topic>Interleukin-1alpha - metabolism</topic><topic>Interleukin-1alpha - pharmacology</topic><topic>Lipid Metabolism - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Hairless</topic><topic>Mice, Knockout</topic><topic>Middle Aged</topic><topic>Models, Animal</topic><topic>Receptors, Interleukin-1 - genetics</topic><topic>Receptors, Interleukin-1 - metabolism</topic><topic>Tacrolimus - administration & dosage</topic><topic>Tacrolimus - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jung, Ye-Jin</creatorcontrib><creatorcontrib>Jung, Minyoung</creatorcontrib><creatorcontrib>Kim, Minjeong</creatorcontrib><creatorcontrib>Hong, Seung-Phil</creatorcontrib><creatorcontrib>Choi, Eung Ho</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><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>Journal of investigative dermatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jung, Ye-Jin</au><au>Jung, Minyoung</au><au>Kim, Minjeong</au><au>Hong, Seung-Phil</au><au>Choi, Eung Ho</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IL-1α Stimulation Restores Epidermal Permeability and Antimicrobial Barriers Compromised by Topical Tacrolimus</atitle><jtitle>Journal of investigative dermatology</jtitle><addtitle>J Invest Dermatol</addtitle><date>2011-03-01</date><risdate>2011</risdate><volume>131</volume><issue>3</issue><spage>698</spage><epage>705</epage><pages>698-705</pages><issn>0022-202X</issn><eissn>1523-1747</eissn><coden>JIDEAE</coden><abstract>In a previous study, we showed that barrier recovery was delayed after acute barrier disruption in the skin treated with topical calcineurin inhibitors. Tacrolimus decreases lipid synthesis and the expressions of antimicrobial peptide (AMP) and IL-1α in the epidermis. IL-1α is an important cytokine for improving barrier function, lamellar body (LB) production, and lipid synthesis in keratinocytes (KCs). We aimed to evaluate whether IL-1α stimulation could restore the barrier dysfunction observed in tacrolimus-treated skin. Topical imiquimod, an IL-1α inducer, restored the epidermal permeability barrier recovery that had been inhibited by tacrolimus treatment in human (n=15) and murine (n=10) skins, and improved stratum corneum integrity by restoring corneodosmosomes in murine skin (n=6). Imiquimod co-applied on the epidermis resulted in an increase in the production of LB and three major lipid synthesis-related enzymes, and in the expressions of mBD3, CRAMP, and IL-1α (n=5). Furthermore, intracutaneous injection of IL-1α restored permeability barrier recovery (n=6). In IL-1 type 1 receptor knockout mice, topical imiquimod was unable to restore permeability barrier recovery after tacrolimus treatment (n=21). In conclusion, IL-1α stimulation induced positive effects on epidermal permeability and antimicrobial barrier functions in tacrolimus-treated skin. These positive effects were mediated by an increase in epidermal lipid synthesis, LB production, and AMP expression.
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| subjects | Administration, Topical Adult Aminoquinolines - administration & dosage Aminoquinolines - pharmacology Animals Antimicrobial Cationic Peptides beta-Defensins - metabolism Biological and medical sciences Cathelicidins - metabolism Cell Membrane - drug effects Cell Membrane - microbiology Cell Membrane Permeability - drug effects Cell Membrane Permeability - physiology Dermatology Desmosomes - drug effects Desmosomes - physiology Epidermal Cells Epidermis - drug effects Epidermis - metabolism Female Humans Imiquimod Immunosuppressive Agents - administration & dosage Immunosuppressive Agents - pharmacology Interleukin-1alpha - agonists Interleukin-1alpha - metabolism Interleukin-1alpha - pharmacology Lipid Metabolism - drug effects Male Medical sciences Mice Mice, Hairless Mice, Knockout Middle Aged Models, Animal Receptors, Interleukin-1 - genetics Receptors, Interleukin-1 - metabolism Tacrolimus - administration & dosage Tacrolimus - pharmacology |
| title | IL-1α Stimulation Restores Epidermal Permeability and Antimicrobial Barriers Compromised by Topical Tacrolimus |
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