dinoprost and Virus-Diseases

Intrauterine infection caused by viral infection has been implicated to contribute to preterm birth. Hepatitis A virus cellular receptor 2 (HAVCR2) regulates inflammation in non-gestational tissues in response to viral infection.. The aims of this study were to determine the effect of: (i) viral dsRNA analogue polyinosinic:polycytidylic acid (poly(I:C)) on HAVCR2 expression; and (ii) HAVCR2 silencing by siRNA (siHAVCR2) in primary amnion and myometrial cells on poly(I:C)-induced inflammation.. In human foetal membranes and myometrium, HAVCR2 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, IL1A, IL1B and IL6; the expression of chemokines CXCL8 and CCL2; the expression and secretion of adhesion molecules ICAM1 and VCAM1; and PTGS2 and PTGFR mRNA expression and the release of prostaglandin PGF. Collectively, our data suggest that HAVCR2 regulates cytokines, chemokines, prostaglandins and cell adhesion molecules in the presence of viral infection. This suggests a potential for HAVCR2 activators as therapeutics for the management of preterm birth associated with viral infections.

Topics: Adolescent; Adult; Cyclooxygenase 2; Cytokines; Dinoprost; Extraembryonic Membranes; Female; Hepatitis A Virus Cellular Receptor 2; Humans; Intercellular Adhesion Molecule-1; Myometrium; Obstetric Labor, Premature; Poly I-C; Pregnancy; Pregnancy Complications, Infectious; Receptors, Prostaglandin; RNA, Messenger; RNA, Small Interfering; Vascular Cell Adhesion Molecule-1; Virus Diseases; Young Adult