Interferon-γ IFN-γ and a type I IFN (spl IFN) are transiently coexpressed by trophoblastic cells of pig conceptuses at implantation between day 12 and day 20 of gestation. The local effects of these trophoblastic IFNs were examined on endometrial cells and on trophoblast by measuring antiviral activity and the induction of (2′,5′)-oligoadenylate synthetase activity. Trophoblastic vesicles were shown to be susceptible to infection by vesicular stomatitis virus and transmissible gastroenteritis virus. Vesicular stomatitis virus multiplied by about 1000 times in trophoblastic vesicles, and endogenous trophoblastic IFNs or exogenous recombinant IFN-γ or spl IFN had no effect on virus production. No (2′,5′)-oligoadenylate synthetase activity could be measured on the trophoblast, even after treatment with IFN-γ or spl IFN. These results clearly show that trophoblastic IFNs cannot induce antiviral resistance or (2′,5′)-oligoadenylate synthetase activity in the trophoblast, suggesting that these IFNs have no autocrine function. Endometrial epithelial and stromal cells in primary cultures displayed distinct sensitivity to the antiviral effect of IFN-γ and spl IFN. Stromal fibroblasts were highly sensitive to spl IFN but weakly sensitive to IFN-γ; epithelial cells were sensitive to both IFNs. The same sensitivity pattern was obtained when measuring the (2′,5′)-oligoadenylate synthetase activity. Flushing fluid, containing IFN-γ and type I IFN, was a potent inducer of antiviral effect and (2′,5′)-oligoadenylate synthetase activity. It is therefore postulated that the endometrial epithelium is the most likely target of trophoblastic IFNs. It is possible that these IFNs play a role in the viral protection of conceptuses.
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