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Hepatitis A virus cellular receptor 2 ( HAVCR 2) is decreased with viral infection and regulates pro‐labour mediators OA
Author(s) -
Liong Stella,
Lim Ratana,
Barker Gillian,
Lappas Martha
Publication year - 2017
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12696
Subject(s) - chemokine , amnion , biology , inflammation , receptor , cell adhesion molecule , viral entry , proinflammatory cytokine , transfection , immunology , virus , microbiology and biotechnology , viral replication , cell culture , fetus , pregnancy , biochemistry , genetics
Problem Intrauterine infection caused by viral infection has been implicated to contribute to preterm birth. Hepatitis A virus cellular receptor 2 ( HAVCR 2) regulates inflammation in non‐gestational tissues in response to viral infection. Method of study The aims of this study were to determine the effect of: (i) viral ds RNA analogue polyinosinic:polycytidylic acid (poly(I:C)) on HAVCR 2 expression; and (ii) HAVCR 2 silencing by si RNA (si HAVCR 2) in primary amnion and myometrial cells on poly(I:C)‐induced inflammation. Results In human foetal membranes and myometrium, HAVCR 2 mRNA and protein expression was decreased when exposed to poly(I:C). Treatment of primary amnion and myometrial cells with poly(I:C) significantly increased the expression and release of pro‐inflammatory cytokines TNF , IL 1A , IL 1B and IL 6 ; the expression of chemokines CXCL 8 and CCL 2 ; the expression and secretion of adhesion molecules ICAM 1 and VCAM 1 ; and PTGS 2 and PTGFR mRNA expression and the release of prostaglandin PGF 2α . This increase was significantly augmented in cells transfected with si HAVCR 2. Furthermore, mRNA expression of anti‐inflammatory cytokines IL 4 and IL 10 was significantly decreased. Conclusion Collectively, our data suggest that HAVCR 2 regulates cytokines, chemokines, prostaglandins and cell adhesion molecules in the presence of viral infection. This suggests a potential for HAVCR 2 activators as therapeutics for the management of preterm birth associated with viral infections.