학술논문
IL-36γ Augments Host Defense and Immune Responses in Human Female Reproductive Tract Epithelial Cells.
Document Type
Academic Journal
Author
Winkle SM; Department of Basic Medical Sciences, College of Medicine-Phoenix, University of Arizona, Phoenix AZ, USA.; Throop AL; Department of Basic Medical Sciences, College of Medicine-Phoenix, University of Arizona, Phoenix AZ, USA.; Herbst-Kralovetz MM; Department of Basic Medical Sciences, College of Medicine-Phoenix, University of Arizona, Phoenix AZ, USA.
Source
Publisher: Frontiers Research Foundation Country of Publication: Switzerland NLM ID: 101548977 Publication Model: eCollection Cited Medium: Print ISSN: 1664-302X (Print) Linking ISSN: 1664302X NLM ISO Abbreviation: Front Microbiol Subsets: PubMed not MEDLINE
Subject
Language
English
ISSN
1664-302X
Abstract
IL-36γ 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-36γ 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-36γ and its receptor was determined. Polyinosinic-polycytidylic acid (poly I:C), flagellin, and synthetic lipoprotein (FSL-1) significantly induced expression of IL-36γ in a dose-dependent manner, and appeared to be TLR-dependent. Recombinant IL-36γ treatment resulted in self-amplification of IL-36γ 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-36γ are present in the human FRT EC and that they are differentially induced by microbial products at this site. We conclude that IL-36γ 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.