IL-36γ Augments Host Defense and Immune Responses in Human Female Reproductive Tract Epithelial Cells

Persistent Link:
http://hdl.handle.net/10150/617371
Title:
IL-36γ Augments Host Defense and Immune Responses in Human Female Reproductive Tract Epithelial Cells
Author:
Winkle, Sean M.; Throop, Andrea L.; Herbst-Kralovetz, Melissa M.
Affiliation:
Univ Arizona, Coll Med Phoenix, Dept Basic Med Sci
Issue Date:
2016-06-17
Publisher:
FRONTIERS MEDIA SA
Citation:
IL-36γ Augments Host Defense and Immune Responses in Human Female Reproductive Tract Epithelial Cells 2016, 7 Frontiers in Microbiology
Journal:
Frontiers in Microbiology
Rights:
Copyright © 2016 Winkle, Throop and Herbst-Kralovetz. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).
Collection Information:
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.
Abstract:
IL-36 gamma is a proinflamatory cytokine which belongs to the IL-1 family of cytokines. It is expressed in the skin and by epithelial cells (ECs) lining lung and gut tissue. We used human 3-D organotypic cells, that recapitulate either in vivo human vaginal or cervical tissue, to explore the possible role of IL-36 gamma in host defense against pathogens in the human female reproductive tract (FRT). EC were exposed to compounds derived from virus or bacterial sources and induction and regulation of IL-36 gamma and its receptor was determined. Polyinosinic-polycytidylic acid (poly I:C), flagellin, and synthetic lipoprotein (FSL-1) significantly induced expression of IL-36 gamma in a dose-dependent manner, and appeared to be TLR-dependent. Recombinant IL-36 gamma treatment resulted in self amplification of IL-36 gamma and its receptor (IL-36R) via increased gene expression, and promoted other inflammatory signaling pathways. This is the first report to demonstrate that the IL-36 receptor and IL-36 gamma are present in the human FRT EC and that they are differentially induced by microbial products at this site. We conclude that IL-36 gamma is a driver for epithelial and immune activation following microbial insult and, as such, may play a critical role in host defense in the FRT.
Note:
Open access.
ISSN:
1664-302X
DOI:
10.3389/fmicb.2016.00955
Keywords:
IL-1 family; IL-36 gamma; human epithelial cells; antimicrobial peptides; innate immunity; IL-36 receptor; microbial products; inflammatory mediators
Version:
Final published version
Sponsors:
National Institutes of Health; NIAID [1R15AI113457-01A1]
Additional Links:
http://journal.frontiersin.org/Article/10.3389/fmicb.2016.00955/abstract

Full metadata record

DC FieldValue Language
dc.contributor.authorWinkle, Sean M.en
dc.contributor.authorThroop, Andrea L.en
dc.contributor.authorHerbst-Kralovetz, Melissa M.en
dc.date.accessioned2016-07-23T00:08:55Z-
dc.date.available2016-07-23T00:08:55Z-
dc.date.issued2016-06-17-
dc.identifier.citationIL-36γ Augments Host Defense and Immune Responses in Human Female Reproductive Tract Epithelial Cells 2016, 7 Frontiers in Microbiologyen
dc.identifier.issn1664-302X-
dc.identifier.doi10.3389/fmicb.2016.00955-
dc.identifier.urihttp://hdl.handle.net/10150/617371-
dc.description.abstractIL-36 gamma is a proinflamatory cytokine which belongs to the IL-1 family of cytokines. It is expressed in the skin and by epithelial cells (ECs) lining lung and gut tissue. We used human 3-D organotypic cells, that recapitulate either in vivo human vaginal or cervical tissue, to explore the possible role of IL-36 gamma in host defense against pathogens in the human female reproductive tract (FRT). EC were exposed to compounds derived from virus or bacterial sources and induction and regulation of IL-36 gamma and its receptor was determined. Polyinosinic-polycytidylic acid (poly I:C), flagellin, and synthetic lipoprotein (FSL-1) significantly induced expression of IL-36 gamma in a dose-dependent manner, and appeared to be TLR-dependent. Recombinant IL-36 gamma treatment resulted in self amplification of IL-36 gamma and its receptor (IL-36R) via increased gene expression, and promoted other inflammatory signaling pathways. This is the first report to demonstrate that the IL-36 receptor and IL-36 gamma are present in the human FRT EC and that they are differentially induced by microbial products at this site. We conclude that IL-36 gamma is a driver for epithelial and immune activation following microbial insult and, as such, may play a critical role in host defense in the FRT.en
dc.description.sponsorshipNational Institutes of Health; NIAID [1R15AI113457-01A1]en
dc.language.isoenen
dc.publisherFRONTIERS MEDIA SAen
dc.relation.urlhttp://journal.frontiersin.org/Article/10.3389/fmicb.2016.00955/abstracten
dc.rightsCopyright © 2016 Winkle, Throop and Herbst-Kralovetz. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).en
dc.subjectIL-1 familyen
dc.subjectIL-36 gammaen
dc.subjecthuman epithelial cellsen
dc.subjectantimicrobial peptidesen
dc.subjectinnate immunityen
dc.subjectIL-36 receptoren
dc.subjectmicrobial productsen
dc.subjectinflammatory mediatorsen
dc.titleIL-36γ Augments Host Defense and Immune Responses in Human Female Reproductive Tract Epithelial Cellsen
dc.typeArticleen
dc.contributor.departmentUniv Arizona, Coll Med Phoenix, Dept Basic Med Scien
dc.identifier.journalFrontiers in Microbiologyen
dc.description.noteOpen access.en
dc.description.collectioninformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen
All Items in UA Campus Repository are protected by copyright, with all rights reserved, unless otherwise indicated.