Up-regulation of HMGB1 and TLR4 in skin lesions of lichen planus
Lichen planus (LP) is a chronic, mucocutaneous inflammatory disease of an unknown aetiology. The disease has been associated with certain viruses, and the factors such as DAMPs ( damage-associated molecular patterns ) and PAMPs ( pathogen-associated molecular patterns ) may also contribute to the in...
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Veröffentlicht in: | Archives of Dermatological Research 2018-08, Vol.310 (6), p.523-528 |
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creator | de Carvalho, Gabriel Costa Hirata, Fabiana Yasumoto Araujo Domingues, Rosana Figueiredo, Cristina Adelaide Zaniboni, Mariana Colombini Pereira, Naiura Vieira Sotto, Mirian Nacagami Aoki, Valéria da Silva Duarte, Alberto José Sato, Maria Notomi |
description | Lichen planus (LP) is a chronic, mucocutaneous inflammatory disease of an unknown aetiology. The disease has been associated with certain viruses, and the factors such as DAMPs (
damage-associated molecular patterns
) and PAMPs (
pathogen-associated molecular patterns
) may also contribute to the inflammatory response in LP. HMGB1 (
high mobility group box 1 protein
) is one of the major DAMPs that induces inflammation and could trigger LP disease. The present study was aimed to examine TLR4, RAGE and HMGB1 production in epidermis or dermis by immunohistochemistry and the respective expression of these targets in the skin lesions of patients with LP. Moreover, we measured HMGB1 serum levels by ELISA. The results showed similar profile of expression by HMGB1 and TLR4, which are decreased at epidermis and up-regulated at dermis of skin lesions of LP patients that was sustained by intense cellular infiltration. RAGE expression was also increased in dermis of LP. Although there is increased RAGE protein levels, a decreased RAGE transcript levels was detected. Similar HMGB1 serum levels were detected in the LP and control groups. This study demonstrates that HMGB1 and TLR4 could contribute to the inflammatory LP process in skin. |
doi_str_mv | 10.1007/s00403-018-1837-5 |
format | Article |
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damage-associated molecular patterns
) and PAMPs (
pathogen-associated molecular patterns
) may also contribute to the inflammatory response in LP. HMGB1 (
high mobility group box 1 protein
) is one of the major DAMPs that induces inflammation and could trigger LP disease. The present study was aimed to examine TLR4, RAGE and HMGB1 production in epidermis or dermis by immunohistochemistry and the respective expression of these targets in the skin lesions of patients with LP. Moreover, we measured HMGB1 serum levels by ELISA. The results showed similar profile of expression by HMGB1 and TLR4, which are decreased at epidermis and up-regulated at dermis of skin lesions of LP patients that was sustained by intense cellular infiltration. RAGE expression was also increased in dermis of LP. Although there is increased RAGE protein levels, a decreased RAGE transcript levels was detected. Similar HMGB1 serum levels were detected in the LP and control groups. This study demonstrates that HMGB1 and TLR4 could contribute to the inflammatory LP process in skin.</description><identifier>ISSN: 0340-3696</identifier><identifier>EISSN: 1432-069X</identifier><identifier>DOI: 10.1007/s00403-018-1837-5</identifier><identifier>PMID: 29728859</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Concise Communication ; Dermatology ; Dermis ; Enzyme-linked immunosorbent assay ; Epidermis ; High mobility group proteins ; Histology ; HMGB1 protein ; Immunohistochemistry ; Inflammation ; Lichen planus ; Medicine ; Medicine & Public Health ; Serum levels ; Skin diseases ; TLR4 protein ; Toll-like receptors ; Transcription</subject><ispartof>Archives of Dermatological Research, 2018-08, Vol.310 (6), p.523-528</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2018</rights><rights>Archives of Dermatological Research is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-c3db31b1996dfecb024a3d15da0645343a3542d9480a112414aa223d511375b63</citedby><cites>FETCH-LOGICAL-c372t-c3db31b1996dfecb024a3d15da0645343a3542d9480a112414aa223d511375b63</cites><orcidid>0000-0002-7911-1824</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00403-018-1837-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00403-018-1837-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29728859$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>de Carvalho, Gabriel Costa</creatorcontrib><creatorcontrib>Hirata, Fabiana Yasumoto Araujo</creatorcontrib><creatorcontrib>Domingues, Rosana</creatorcontrib><creatorcontrib>Figueiredo, Cristina Adelaide</creatorcontrib><creatorcontrib>Zaniboni, Mariana Colombini</creatorcontrib><creatorcontrib>Pereira, Naiura Vieira</creatorcontrib><creatorcontrib>Sotto, Mirian Nacagami</creatorcontrib><creatorcontrib>Aoki, Valéria</creatorcontrib><creatorcontrib>da Silva Duarte, Alberto José</creatorcontrib><creatorcontrib>Sato, Maria Notomi</creatorcontrib><title>Up-regulation of HMGB1 and TLR4 in skin lesions of lichen planus</title><title>Archives of Dermatological Research</title><addtitle>Arch Dermatol Res</addtitle><addtitle>Arch Dermatol Res</addtitle><description>Lichen planus (LP) is a chronic, mucocutaneous inflammatory disease of an unknown aetiology. The disease has been associated with certain viruses, and the factors such as DAMPs (
damage-associated molecular patterns
) and PAMPs (
pathogen-associated molecular patterns
) may also contribute to the inflammatory response in LP. HMGB1 (
high mobility group box 1 protein
) is one of the major DAMPs that induces inflammation and could trigger LP disease. The present study was aimed to examine TLR4, RAGE and HMGB1 production in epidermis or dermis by immunohistochemistry and the respective expression of these targets in the skin lesions of patients with LP. Moreover, we measured HMGB1 serum levels by ELISA. The results showed similar profile of expression by HMGB1 and TLR4, which are decreased at epidermis and up-regulated at dermis of skin lesions of LP patients that was sustained by intense cellular infiltration. RAGE expression was also increased in dermis of LP. Although there is increased RAGE protein levels, a decreased RAGE transcript levels was detected. Similar HMGB1 serum levels were detected in the LP and control groups. This study demonstrates that HMGB1 and TLR4 could contribute to the inflammatory LP process in skin.</description><subject>Concise Communication</subject><subject>Dermatology</subject><subject>Dermis</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Epidermis</subject><subject>High mobility group proteins</subject><subject>Histology</subject><subject>HMGB1 protein</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Lichen planus</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Serum levels</subject><subject>Skin diseases</subject><subject>TLR4 protein</subject><subject>Toll-like receptors</subject><subject>Transcription</subject><issn>0340-3696</issn><issn>1432-069X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kM9LwzAUx4Mobsz9AV6k4MVL9OVX29zUoVOYCLKBt5A26ezs2pqsB_97UzoVBHN4OeTzvu_lg9ApgUsCkFx5AA4MA0kxSVmCxQEaE84ohli-HqIxMA6YxTIeoan3GwgnAU4hOUYjKhOapkKO0fWqxc6uu0rvyqaOmiJ6eJrfkkjXJlouXnhU1pF_D6WyPgC-J6oyf7N11Fa67vwJOip05e10f0_Q6v5uOXvAi-f54-xmgXOW0F2oJmMkI1LGprB5BpRrZogwGmIuGGeaCU6N5CloQignXGtKmRGEsERkMZugiyG3dc1HZ_1ObUuf2yosYZvOKwpM0PC9GAJ6_gfdNJ2rw3Y9xQUwCX0gGajcNd47W6jWlVvtPhUB1RtWg2EVDKvesBKh52yf3GVba346vn0GgA6AD0_12rrf0f-nfgFohIGQ</recordid><startdate>20180801</startdate><enddate>20180801</enddate><creator>de Carvalho, Gabriel Costa</creator><creator>Hirata, Fabiana Yasumoto Araujo</creator><creator>Domingues, Rosana</creator><creator>Figueiredo, Cristina Adelaide</creator><creator>Zaniboni, Mariana Colombini</creator><creator>Pereira, Naiura Vieira</creator><creator>Sotto, Mirian Nacagami</creator><creator>Aoki, Valéria</creator><creator>da Silva Duarte, Alberto José</creator><creator>Sato, Maria Notomi</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7911-1824</orcidid></search><sort><creationdate>20180801</creationdate><title>Up-regulation of HMGB1 and TLR4 in skin lesions of lichen planus</title><author>de Carvalho, Gabriel Costa ; Hirata, Fabiana Yasumoto Araujo ; Domingues, Rosana ; Figueiredo, Cristina Adelaide ; Zaniboni, Mariana Colombini ; Pereira, Naiura Vieira ; Sotto, Mirian Nacagami ; Aoki, Valéria ; da Silva Duarte, Alberto José ; Sato, Maria Notomi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-c3db31b1996dfecb024a3d15da0645343a3542d9480a112414aa223d511375b63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Concise Communication</topic><topic>Dermatology</topic><topic>Dermis</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Epidermis</topic><topic>High mobility group proteins</topic><topic>Histology</topic><topic>HMGB1 protein</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Lichen planus</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Serum levels</topic><topic>Skin diseases</topic><topic>TLR4 protein</topic><topic>Toll-like receptors</topic><topic>Transcription</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de Carvalho, Gabriel Costa</creatorcontrib><creatorcontrib>Hirata, Fabiana Yasumoto Araujo</creatorcontrib><creatorcontrib>Domingues, Rosana</creatorcontrib><creatorcontrib>Figueiredo, Cristina Adelaide</creatorcontrib><creatorcontrib>Zaniboni, Mariana Colombini</creatorcontrib><creatorcontrib>Pereira, Naiura Vieira</creatorcontrib><creatorcontrib>Sotto, Mirian Nacagami</creatorcontrib><creatorcontrib>Aoki, Valéria</creatorcontrib><creatorcontrib>da Silva Duarte, Alberto José</creatorcontrib><creatorcontrib>Sato, Maria Notomi</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Archives of Dermatological Research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>de Carvalho, Gabriel Costa</au><au>Hirata, Fabiana Yasumoto Araujo</au><au>Domingues, Rosana</au><au>Figueiredo, Cristina Adelaide</au><au>Zaniboni, Mariana Colombini</au><au>Pereira, Naiura Vieira</au><au>Sotto, Mirian Nacagami</au><au>Aoki, Valéria</au><au>da Silva Duarte, Alberto José</au><au>Sato, Maria Notomi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Up-regulation of HMGB1 and TLR4 in skin lesions of lichen planus</atitle><jtitle>Archives of Dermatological Research</jtitle><stitle>Arch Dermatol Res</stitle><addtitle>Arch Dermatol Res</addtitle><date>2018-08-01</date><risdate>2018</risdate><volume>310</volume><issue>6</issue><spage>523</spage><epage>528</epage><pages>523-528</pages><issn>0340-3696</issn><eissn>1432-069X</eissn><abstract>Lichen planus (LP) is a chronic, mucocutaneous inflammatory disease of an unknown aetiology. The disease has been associated with certain viruses, and the factors such as DAMPs (
damage-associated molecular patterns
) and PAMPs (
pathogen-associated molecular patterns
) may also contribute to the inflammatory response in LP. HMGB1 (
high mobility group box 1 protein
) is one of the major DAMPs that induces inflammation and could trigger LP disease. The present study was aimed to examine TLR4, RAGE and HMGB1 production in epidermis or dermis by immunohistochemistry and the respective expression of these targets in the skin lesions of patients with LP. Moreover, we measured HMGB1 serum levels by ELISA. The results showed similar profile of expression by HMGB1 and TLR4, which are decreased at epidermis and up-regulated at dermis of skin lesions of LP patients that was sustained by intense cellular infiltration. RAGE expression was also increased in dermis of LP. Although there is increased RAGE protein levels, a decreased RAGE transcript levels was detected. Similar HMGB1 serum levels were detected in the LP and control groups. This study demonstrates that HMGB1 and TLR4 could contribute to the inflammatory LP process in skin.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>29728859</pmid><doi>10.1007/s00403-018-1837-5</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-7911-1824</orcidid></addata></record> |
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subjects | Concise Communication Dermatology Dermis Enzyme-linked immunosorbent assay Epidermis High mobility group proteins Histology HMGB1 protein Immunohistochemistry Inflammation Lichen planus Medicine Medicine & Public Health Serum levels Skin diseases TLR4 protein Toll-like receptors Transcription |
title | Up-regulation of HMGB1 and TLR4 in skin lesions of lichen planus |
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