Structural damage in the C. elegans epidermis causes release of STA-2 and induction of an innate immune response
The epidermis constantly encounters invasions that disrupt its architecture, yet whether the epidermal immune system utilizes damaged structures as danger signals to activate self-defense is unclear. Here, we used a C. elegans epidermis model in which skin-penetrating infection or injury activates i...
Gespeichert in:
| Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 2015-02, Vol.42 (2), p.309-320 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 320 |
|---|---|
| container_issue | 2 |
| container_start_page | 309 |
| container_title | Immunity (Cambridge, Mass.) |
| container_volume | 42 |
| creator | Zhang, Yun Li, Wenna Li, Linfeng Li, Yuanbao Fu, Rong Zhu, Yi Li, Jie Zhou, Yanfeng Xiong, Sidong Zhang, Huimin |
| description | The epidermis constantly encounters invasions that disrupt its architecture, yet whether the epidermal immune system utilizes damaged structures as danger signals to activate self-defense is unclear. Here, we used a C. elegans epidermis model in which skin-penetrating infection or injury activates immune defense and antimicrobial peptide (AMP) production. By systemically disrupting each architectural component, we found that only disturbance of the apical hemidesmosomes triggered an immune response and robust AMP expression. The epidermis recognized structural damage through hemidesmosomes associated with a STAT-like protein, whose disruption led to detachment of STA-2 molecules from hemidesmosomes and transcription of AMPs. This machinery enabled the epidermis to bypass certain signaling amplification and directly trigger AMP production when subjected to extensive architectural damage. Together, our findings uncover an evolutionarily conserved mechanism for the epithelial barriers to detect danger and activate immune defense. |
| doi_str_mv | 10.1016/j.immuni.2015.01.014 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1664209786</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1657324484</sourcerecordid><originalsourceid>FETCH-LOGICAL-c344t-f05b2646731dc5c030ece054e88a65a9bcd8ad92d3d90f4aa207ff28b41596043</originalsourceid><addsrcrecordid>eNqNkU2L1TAUhoMozof-A5GAGzetJ59tl8NldIQBFzOuw7nJ6dhLm9akXfjvTbmjC1fCgeQkz_tykpexdwJqAcJ-OtXDNG1xqCUIU4MopV-wSwFdU2nRwst93-iqsUJdsKucT1AI08FrdiGN7WQD-pItD2va_LolHHnACZ-ID5GvP4gfak4jPWHMnJYhUJqGzD1umTJP5QYz8bnnD483leQYQ9GF4jTMcT_GWPqIa7Hbp6QiycscM71hr3ocM719Xq_Z98-3j4e76v7bl6-Hm_vKK63XqgdzlFbbRongjQcF5AmMprZFa7A7-tBi6GRQoYNeI0po-l62Ry1MZ0Gra_bx7Luk-edGeXVlfk_jiJHmLTthrZblr1r7H6hplNS63V0__IOe5i3F8pCdMo0xSkCh9Jnyac45Ue-WNEyYfjkBbg_Pndw5PLeH50CU2s3fP5tvx4nCX9GftNRvOO2WJA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1655755310</pqid></control><display><type>article</type><title>Structural damage in the C. elegans epidermis causes release of STA-2 and induction of an innate immune response</title><source>MEDLINE</source><source>Cell Press Free Archives</source><source>ScienceDirect Journals (5 years ago - present)</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Zhang, Yun ; Li, Wenna ; Li, Linfeng ; Li, Yuanbao ; Fu, Rong ; Zhu, Yi ; Li, Jie ; Zhou, Yanfeng ; Xiong, Sidong ; Zhang, Huimin</creator><creatorcontrib>Zhang, Yun ; Li, Wenna ; Li, Linfeng ; Li, Yuanbao ; Fu, Rong ; Zhu, Yi ; Li, Jie ; Zhou, Yanfeng ; Xiong, Sidong ; Zhang, Huimin</creatorcontrib><description>The epidermis constantly encounters invasions that disrupt its architecture, yet whether the epidermal immune system utilizes damaged structures as danger signals to activate self-defense is unclear. Here, we used a C. elegans epidermis model in which skin-penetrating infection or injury activates immune defense and antimicrobial peptide (AMP) production. By systemically disrupting each architectural component, we found that only disturbance of the apical hemidesmosomes triggered an immune response and robust AMP expression. The epidermis recognized structural damage through hemidesmosomes associated with a STAT-like protein, whose disruption led to detachment of STA-2 molecules from hemidesmosomes and transcription of AMPs. This machinery enabled the epidermis to bypass certain signaling amplification and directly trigger AMP production when subjected to extensive architectural damage. Together, our findings uncover an evolutionarily conserved mechanism for the epithelial barriers to detect danger and activate immune defense.</description><identifier>ISSN: 1074-7613</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/j.immuni.2015.01.014</identifier><identifier>PMID: 25692704</identifier><language>eng</language><publisher>United States: Elsevier Limited</publisher><subject>Animals ; Antimicrobial Cationic Peptides - biosynthesis ; Antimicrobial Cationic Peptides - genetics ; Architecture ; Caenorhabditis elegans - immunology ; Caenorhabditis elegans Proteins - immunology ; Caenorhabditis elegans Proteins - metabolism ; Cell Adhesion Molecules - immunology ; Cells, Cultured ; Epidermis - immunology ; Epidermis - injuries ; Experiments ; Gene expression ; Hemidesmosomes - immunology ; Hemidesmosomes - pathology ; Humans ; Immune system ; Immunity, Innate ; Keratinocytes - immunology ; Keratinocytes - metabolism ; Nematodes ; p38 Mitogen-Activated Protein Kinases - immunology ; Proteins ; Signal Transduction - immunology ; Skin ; STAT Transcription Factors - metabolism ; Worms ; Wound healing</subject><ispartof>Immunity (Cambridge, Mass.), 2015-02, Vol.42 (2), p.309-320</ispartof><rights>Copyright © 2015 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Feb 17, 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c344t-f05b2646731dc5c030ece054e88a65a9bcd8ad92d3d90f4aa207ff28b41596043</citedby><cites>FETCH-LOGICAL-c344t-f05b2646731dc5c030ece054e88a65a9bcd8ad92d3d90f4aa207ff28b41596043</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25692704$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yun</creatorcontrib><creatorcontrib>Li, Wenna</creatorcontrib><creatorcontrib>Li, Linfeng</creatorcontrib><creatorcontrib>Li, Yuanbao</creatorcontrib><creatorcontrib>Fu, Rong</creatorcontrib><creatorcontrib>Zhu, Yi</creatorcontrib><creatorcontrib>Li, Jie</creatorcontrib><creatorcontrib>Zhou, Yanfeng</creatorcontrib><creatorcontrib>Xiong, Sidong</creatorcontrib><creatorcontrib>Zhang, Huimin</creatorcontrib><title>Structural damage in the C. elegans epidermis causes release of STA-2 and induction of an innate immune response</title><title>Immunity (Cambridge, Mass.)</title><addtitle>Immunity</addtitle><description>The epidermis constantly encounters invasions that disrupt its architecture, yet whether the epidermal immune system utilizes damaged structures as danger signals to activate self-defense is unclear. Here, we used a C. elegans epidermis model in which skin-penetrating infection or injury activates immune defense and antimicrobial peptide (AMP) production. By systemically disrupting each architectural component, we found that only disturbance of the apical hemidesmosomes triggered an immune response and robust AMP expression. The epidermis recognized structural damage through hemidesmosomes associated with a STAT-like protein, whose disruption led to detachment of STA-2 molecules from hemidesmosomes and transcription of AMPs. This machinery enabled the epidermis to bypass certain signaling amplification and directly trigger AMP production when subjected to extensive architectural damage. Together, our findings uncover an evolutionarily conserved mechanism for the epithelial barriers to detect danger and activate immune defense.</description><subject>Animals</subject><subject>Antimicrobial Cationic Peptides - biosynthesis</subject><subject>Antimicrobial Cationic Peptides - genetics</subject><subject>Architecture</subject><subject>Caenorhabditis elegans - immunology</subject><subject>Caenorhabditis elegans Proteins - immunology</subject><subject>Caenorhabditis elegans Proteins - metabolism</subject><subject>Cell Adhesion Molecules - immunology</subject><subject>Cells, Cultured</subject><subject>Epidermis - immunology</subject><subject>Epidermis - injuries</subject><subject>Experiments</subject><subject>Gene expression</subject><subject>Hemidesmosomes - immunology</subject><subject>Hemidesmosomes - pathology</subject><subject>Humans</subject><subject>Immune system</subject><subject>Immunity, Innate</subject><subject>Keratinocytes - immunology</subject><subject>Keratinocytes - metabolism</subject><subject>Nematodes</subject><subject>p38 Mitogen-Activated Protein Kinases - immunology</subject><subject>Proteins</subject><subject>Signal Transduction - immunology</subject><subject>Skin</subject><subject>STAT Transcription Factors - metabolism</subject><subject>Worms</subject><subject>Wound healing</subject><issn>1074-7613</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU2L1TAUhoMozof-A5GAGzetJ59tl8NldIQBFzOuw7nJ6dhLm9akXfjvTbmjC1fCgeQkz_tykpexdwJqAcJ-OtXDNG1xqCUIU4MopV-wSwFdU2nRwst93-iqsUJdsKucT1AI08FrdiGN7WQD-pItD2va_LolHHnACZ-ID5GvP4gfak4jPWHMnJYhUJqGzD1umTJP5QYz8bnnD483leQYQ9GF4jTMcT_GWPqIa7Hbp6QiycscM71hr3ocM719Xq_Z98-3j4e76v7bl6-Hm_vKK63XqgdzlFbbRongjQcF5AmMprZFa7A7-tBi6GRQoYNeI0po-l62Ry1MZ0Gra_bx7Luk-edGeXVlfk_jiJHmLTthrZblr1r7H6hplNS63V0__IOe5i3F8pCdMo0xSkCh9Jnyac45Ue-WNEyYfjkBbg_Pndw5PLeH50CU2s3fP5tvx4nCX9GftNRvOO2WJA</recordid><startdate>20150217</startdate><enddate>20150217</enddate><creator>Zhang, Yun</creator><creator>Li, Wenna</creator><creator>Li, Linfeng</creator><creator>Li, Yuanbao</creator><creator>Fu, Rong</creator><creator>Zhu, Yi</creator><creator>Li, Jie</creator><creator>Zhou, Yanfeng</creator><creator>Xiong, Sidong</creator><creator>Zhang, Huimin</creator><general>Elsevier Limited</general><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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20150217</creationdate><title>Structural damage in the C. elegans epidermis causes release of STA-2 and induction of an innate immune response</title><author>Zhang, Yun ; Li, Wenna ; Li, Linfeng ; Li, Yuanbao ; Fu, Rong ; Zhu, Yi ; Li, Jie ; Zhou, Yanfeng ; Xiong, Sidong ; Zhang, Huimin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c344t-f05b2646731dc5c030ece054e88a65a9bcd8ad92d3d90f4aa207ff28b41596043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Antimicrobial Cationic Peptides - biosynthesis</topic><topic>Antimicrobial Cationic Peptides - genetics</topic><topic>Architecture</topic><topic>Caenorhabditis elegans - immunology</topic><topic>Caenorhabditis elegans Proteins - immunology</topic><topic>Caenorhabditis elegans Proteins - metabolism</topic><topic>Cell Adhesion Molecules - immunology</topic><topic>Cells, Cultured</topic><topic>Epidermis - immunology</topic><topic>Epidermis - injuries</topic><topic>Experiments</topic><topic>Gene expression</topic><topic>Hemidesmosomes - immunology</topic><topic>Hemidesmosomes - pathology</topic><topic>Humans</topic><topic>Immune system</topic><topic>Immunity, Innate</topic><topic>Keratinocytes - immunology</topic><topic>Keratinocytes - metabolism</topic><topic>Nematodes</topic><topic>p38 Mitogen-Activated Protein Kinases - immunology</topic><topic>Proteins</topic><topic>Signal Transduction - immunology</topic><topic>Skin</topic><topic>STAT Transcription Factors - metabolism</topic><topic>Worms</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Yun</creatorcontrib><creatorcontrib>Li, Wenna</creatorcontrib><creatorcontrib>Li, Linfeng</creatorcontrib><creatorcontrib>Li, Yuanbao</creatorcontrib><creatorcontrib>Fu, Rong</creatorcontrib><creatorcontrib>Zhu, Yi</creatorcontrib><creatorcontrib>Li, Jie</creatorcontrib><creatorcontrib>Zhou, Yanfeng</creatorcontrib><creatorcontrib>Xiong, Sidong</creatorcontrib><creatorcontrib>Zhang, Huimin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Immunity (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Yun</au><au>Li, Wenna</au><au>Li, Linfeng</au><au>Li, Yuanbao</au><au>Fu, Rong</au><au>Zhu, Yi</au><au>Li, Jie</au><au>Zhou, Yanfeng</au><au>Xiong, Sidong</au><au>Zhang, Huimin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Structural damage in the C. elegans epidermis causes release of STA-2 and induction of an innate immune response</atitle><jtitle>Immunity (Cambridge, Mass.)</jtitle><addtitle>Immunity</addtitle><date>2015-02-17</date><risdate>2015</risdate><volume>42</volume><issue>2</issue><spage>309</spage><epage>320</epage><pages>309-320</pages><issn>1074-7613</issn><eissn>1097-4180</eissn><abstract>The epidermis constantly encounters invasions that disrupt its architecture, yet whether the epidermal immune system utilizes damaged structures as danger signals to activate self-defense is unclear. Here, we used a C. elegans epidermis model in which skin-penetrating infection or injury activates immune defense and antimicrobial peptide (AMP) production. By systemically disrupting each architectural component, we found that only disturbance of the apical hemidesmosomes triggered an immune response and robust AMP expression. The epidermis recognized structural damage through hemidesmosomes associated with a STAT-like protein, whose disruption led to detachment of STA-2 molecules from hemidesmosomes and transcription of AMPs. This machinery enabled the epidermis to bypass certain signaling amplification and directly trigger AMP production when subjected to extensive architectural damage. Together, our findings uncover an evolutionarily conserved mechanism for the epithelial barriers to detect danger and activate immune defense.</abstract><cop>United States</cop><pub>Elsevier Limited</pub><pmid>25692704</pmid><doi>10.1016/j.immuni.2015.01.014</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1074-7613 |
| ispartof | Immunity (Cambridge, Mass.), 2015-02, Vol.42 (2), p.309-320 |
| issn | 1074-7613 1097-4180 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1664209786 |
| source | MEDLINE; Cell Press Free Archives; ScienceDirect Journals (5 years ago - present); EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Antimicrobial Cationic Peptides - biosynthesis Antimicrobial Cationic Peptides - genetics Architecture Caenorhabditis elegans - immunology Caenorhabditis elegans Proteins - immunology Caenorhabditis elegans Proteins - metabolism Cell Adhesion Molecules - immunology Cells, Cultured Epidermis - immunology Epidermis - injuries Experiments Gene expression Hemidesmosomes - immunology Hemidesmosomes - pathology Humans Immune system Immunity, Innate Keratinocytes - immunology Keratinocytes - metabolism Nematodes p38 Mitogen-Activated Protein Kinases - immunology Proteins Signal Transduction - immunology Skin STAT Transcription Factors - metabolism Worms Wound healing |
| title | Structural damage in the C. elegans epidermis causes release of STA-2 and induction of an innate immune response |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T08%3A26%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Structural%20damage%20in%20the%20C.%20elegans%20epidermis%20causes%20release%20of%20STA-2%20and%20induction%20of%20an%20innate%20immune%20response&rft.jtitle=Immunity%20(Cambridge,%20Mass.)&rft.au=Zhang,%20Yun&rft.date=2015-02-17&rft.volume=42&rft.issue=2&rft.spage=309&rft.epage=320&rft.pages=309-320&rft.issn=1074-7613&rft.eissn=1097-4180&rft_id=info:doi/10.1016/j.immuni.2015.01.014&rft_dat=%3Cproquest_cross%3E1657324484%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1655755310&rft_id=info:pmid/25692704&rfr_iscdi=true |