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Production and regulation of interleukin-1 family cytokines at the materno-fetal interface
Cytokine, Volume: 99, Pages: 194 - 202
Swansea University Authors: April Rees , Aled Bryant , Ruth Jones , Cathy Thornton
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DOI (Published version): 10.1016/j.cyto.2017.07.005
Abstract
IL-1 family members regulate innate immune responses, are produced by gestation-associated tissues, and have a role in healthy and adverse pregnancy outcomes. To better understand their role at the materno-fetal interface we used a human tissue explant model to map lipopolysaccharide (LPS)-stimulate...
Published in: | Cytokine |
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ISSN: | 10434666 |
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2017
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URI: | https://cronfa.swan.ac.uk/Record/cronfa34588 |
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To better understand their role at the materno-fetal interface we used a human tissue explant model to map lipopolysaccharide (LPS)-stimulated production of IL-1α, IL-1β, IL-18, IL-33, IL-1Ra, IL-18BPa, ST2 and IL-1RAcP by placenta, choriodecidua and amnion. Caspase-dependent processing of IL-1α, IL-1β, IL-18, and IL-33 and the ability of IL-1α, IL-1β, IL-18, and IL-33 to regulate the production of IL-1RA, IL-18BPa, ST2 and IL-1RAcP was also determined. LPS acted as a potent inducer of IL-1 family member expression especially in the placenta and choriodecidua with the response by the amnion restricted to IL-1β. Caspases-1, 4 and 8 contributed to LPS-stimulated production of IL-1 and IL-18, whereas calpain was required for IL-1 production. Exogenous administration of IL-1α, IL-1β, IL-18, and IL-33 lead to differential expression of IL-1Ra, IL-18BPa, ST2 and IL-1RAcP across all tissues examined. Most notable were the counter-regulatory effect of LPS on IL-1 and IL-1Ra in the amnion and the broad responsiveness of the amnion to IL-1 family cytokines for increased production of immunomodulatory peptides and soluble receptors. The placenta and membranes vary not only in their output of various IL-1 family members but also in their counter-regulatory mechanisms through endogenous inhibitory peptides, processing enzymes and soluble decoy receptors. This interactive network of inflammatory mediators likely contributes to innate defence mechanisms at the materno-fetal interface to limit, in particular, the detrimental effects of microbial invasion.</abstract><type>Journal Article</type><journal>Cytokine</journal><volume>99</volume><paginationStart>194</paginationStart><paginationEnd>202</paginationEnd><publisher/><issnPrint>10434666</issnPrint><keywords>Cytokines, IL-1 family, Placenta, Preterm labour, Reproductive Immunology.</keywords><publishedDay>1</publishedDay><publishedMonth>11</publishedMonth><publishedYear>2017</publishedYear><publishedDate>2017-11-01</publishedDate><doi>10.1016/j.cyto.2017.07.005</doi><url/><notes/><college>COLLEGE NANME</college><department>Medical School</department><CollegeCode>COLLEGE CODE</CollegeCode><DepartmentCode>MEDS</DepartmentCode><institution>Swansea University</institution><apcterm/><lastEdited>2020-05-28T15:21:00.0381212</lastEdited><Created>2017-07-10T11:39:33.3564507</Created><path><level id="1">Faculty of Medicine, Health and Life Sciences</level><level id="2">Swansea University Medical School - Medicine</level></path><authors><author><firstname>April</firstname><surname>Rees</surname><orcid>0000-0002-4408-634X</orcid><order>1</order></author><author><firstname>Louis M.</firstname><surname>Scott</surname><order>2</order></author><author><firstname>Aled</firstname><surname>Bryant</surname><orcid>0000-0002-4650-4672</orcid><order>3</order></author><author><firstname>April</firstname><surname>Rees</surname><order>4</order></author><author><firstname>Billy</firstname><surname>Down</surname><order>5</order></author><author><firstname>Ruth</firstname><surname>Jones</surname><orcid>0000-0001-5811-8827</orcid><order>6</order></author><author><firstname>Cathy</firstname><surname>Thornton</surname><orcid>0000-0002-5153-573X</orcid><order>7</order></author></authors><documents><document><filename>0034588-02082017152533.pdf</filename><originalFilename>34588.pdf</originalFilename><uploaded>2017-08-02T15:25:33.3630000</uploaded><type>Output</type><contentLength>836451</contentLength><contentType>application/pdf</contentType><version>Accepted Manuscript</version><cronfaStatus>true</cronfaStatus><embargoDate>2018-07-18T00:00:00.0000000</embargoDate><copyrightCorrect>true</copyrightCorrect><language>eng</language></document></documents><OutputDurs/></rfc1807> |
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2020-05-28T15:21:00.0381212 v2 34588 2017-07-10 Production and regulation of interleukin-1 family cytokines at the materno-fetal interface ae088f7f8609d2b2ea4666f9b52b3c15 0000-0002-4408-634X April Rees April Rees true false 021f7adc0923f6d2c2e2fc269758b8fe 0000-0002-4650-4672 Aled Bryant Aled Bryant true false a1a281c8720685c422892ef168d4b279 0000-0001-5811-8827 Ruth Jones Ruth Jones true false c71a7a4be7361094d046d312202bce0c 0000-0002-5153-573X Cathy Thornton Cathy Thornton true false 2017-07-10 MEDS IL-1 family members regulate innate immune responses, are produced by gestation-associated tissues, and have a role in healthy and adverse pregnancy outcomes. To better understand their role at the materno-fetal interface we used a human tissue explant model to map lipopolysaccharide (LPS)-stimulated production of IL-1α, IL-1β, IL-18, IL-33, IL-1Ra, IL-18BPa, ST2 and IL-1RAcP by placenta, choriodecidua and amnion. Caspase-dependent processing of IL-1α, IL-1β, IL-18, and IL-33 and the ability of IL-1α, IL-1β, IL-18, and IL-33 to regulate the production of IL-1RA, IL-18BPa, ST2 and IL-1RAcP was also determined. LPS acted as a potent inducer of IL-1 family member expression especially in the placenta and choriodecidua with the response by the amnion restricted to IL-1β. Caspases-1, 4 and 8 contributed to LPS-stimulated production of IL-1 and IL-18, whereas calpain was required for IL-1 production. Exogenous administration of IL-1α, IL-1β, IL-18, and IL-33 lead to differential expression of IL-1Ra, IL-18BPa, ST2 and IL-1RAcP across all tissues examined. Most notable were the counter-regulatory effect of LPS on IL-1 and IL-1Ra in the amnion and the broad responsiveness of the amnion to IL-1 family cytokines for increased production of immunomodulatory peptides and soluble receptors. The placenta and membranes vary not only in their output of various IL-1 family members but also in their counter-regulatory mechanisms through endogenous inhibitory peptides, processing enzymes and soluble decoy receptors. This interactive network of inflammatory mediators likely contributes to innate defence mechanisms at the materno-fetal interface to limit, in particular, the detrimental effects of microbial invasion. Journal Article Cytokine 99 194 202 10434666 Cytokines, IL-1 family, Placenta, Preterm labour, Reproductive Immunology. 1 11 2017 2017-11-01 10.1016/j.cyto.2017.07.005 COLLEGE NANME Medical School COLLEGE CODE MEDS Swansea University 2020-05-28T15:21:00.0381212 2017-07-10T11:39:33.3564507 Faculty of Medicine, Health and Life Sciences Swansea University Medical School - Medicine April Rees 0000-0002-4408-634X 1 Louis M. Scott 2 Aled Bryant 0000-0002-4650-4672 3 April Rees 4 Billy Down 5 Ruth Jones 0000-0001-5811-8827 6 Cathy Thornton 0000-0002-5153-573X 7 0034588-02082017152533.pdf 34588.pdf 2017-08-02T15:25:33.3630000 Output 836451 application/pdf Accepted Manuscript true 2018-07-18T00:00:00.0000000 true eng |
title |
Production and regulation of interleukin-1 family cytokines at the materno-fetal interface |
spellingShingle |
Production and regulation of interleukin-1 family cytokines at the materno-fetal interface April Rees Aled Bryant Ruth Jones Cathy Thornton |
title_short |
Production and regulation of interleukin-1 family cytokines at the materno-fetal interface |
title_full |
Production and regulation of interleukin-1 family cytokines at the materno-fetal interface |
title_fullStr |
Production and regulation of interleukin-1 family cytokines at the materno-fetal interface |
title_full_unstemmed |
Production and regulation of interleukin-1 family cytokines at the materno-fetal interface |
title_sort |
Production and regulation of interleukin-1 family cytokines at the materno-fetal interface |
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ae088f7f8609d2b2ea4666f9b52b3c15 021f7adc0923f6d2c2e2fc269758b8fe a1a281c8720685c422892ef168d4b279 c71a7a4be7361094d046d312202bce0c |
author_id_fullname_str_mv |
ae088f7f8609d2b2ea4666f9b52b3c15_***_April Rees 021f7adc0923f6d2c2e2fc269758b8fe_***_Aled Bryant a1a281c8720685c422892ef168d4b279_***_Ruth Jones c71a7a4be7361094d046d312202bce0c_***_Cathy Thornton |
author |
April Rees Aled Bryant Ruth Jones Cathy Thornton |
author2 |
April Rees Louis M. Scott Aled Bryant April Rees Billy Down Ruth Jones Cathy Thornton |
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description |
IL-1 family members regulate innate immune responses, are produced by gestation-associated tissues, and have a role in healthy and adverse pregnancy outcomes. To better understand their role at the materno-fetal interface we used a human tissue explant model to map lipopolysaccharide (LPS)-stimulated production of IL-1α, IL-1β, IL-18, IL-33, IL-1Ra, IL-18BPa, ST2 and IL-1RAcP by placenta, choriodecidua and amnion. Caspase-dependent processing of IL-1α, IL-1β, IL-18, and IL-33 and the ability of IL-1α, IL-1β, IL-18, and IL-33 to regulate the production of IL-1RA, IL-18BPa, ST2 and IL-1RAcP was also determined. LPS acted as a potent inducer of IL-1 family member expression especially in the placenta and choriodecidua with the response by the amnion restricted to IL-1β. Caspases-1, 4 and 8 contributed to LPS-stimulated production of IL-1 and IL-18, whereas calpain was required for IL-1 production. Exogenous administration of IL-1α, IL-1β, IL-18, and IL-33 lead to differential expression of IL-1Ra, IL-18BPa, ST2 and IL-1RAcP across all tissues examined. Most notable were the counter-regulatory effect of LPS on IL-1 and IL-1Ra in the amnion and the broad responsiveness of the amnion to IL-1 family cytokines for increased production of immunomodulatory peptides and soluble receptors. The placenta and membranes vary not only in their output of various IL-1 family members but also in their counter-regulatory mechanisms through endogenous inhibitory peptides, processing enzymes and soluble decoy receptors. This interactive network of inflammatory mediators likely contributes to innate defence mechanisms at the materno-fetal interface to limit, in particular, the detrimental effects of microbial invasion. |
published_date |
2017-11-01T04:21:55Z |
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11.293348 |