Key result
HAVCR2 silencing significantly augmented poly(I:C)-induced pro-inflammatory cytokine release in primary amnion and myometrial cells, suggesting HAVCR2 regulates inflammation during viral infection.
HAVCR2 regulates inflammatory mediators in response to viral infection in gestational tissues, suggesting HAVCR2 activators could be potential therapeutics for preterm birth.
Supports HAVCR2 as regulator of viral inflammation in gestational tissues; leaves open activator potential for preterm birth prevention.
Problem 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. Method of study 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. Results 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 PGF2α. This increase was significantly augmented in cells transfected with siHAVCR2. Furthermore, mRNA expression of anti‐inflammatory cytokines IL4 and IL10 was significantly decreased. Conclusion 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.
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Liong et al. (2017) studied Preterm birth associated with viral infection. poly(I:C) and HAVCR2 silencing by siRNA was evaluated on HAVCR2 expression and pro-inflammatory cytokine release. HAVCR2 silencing significantly augmented poly(I:C)-induced pro-inflammatory cytokine release in primary amnion and myometrial cells, suggesting HAVCR2 regulates inflammation during viral infection.
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