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Journal of Dairy Science Vol. 79 No. 8 1375-1384
© 1996 by American Dairy Science Association ®
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Treatment with Recombinant Bovine Interferon-tau In Utero Attenuates Secretion of Prostaglandin F from Cultured Endometrial Epithelial Cells

M. D. Meyer 1, G. D. Desnoyers 1, B. Oldick 1, W. W. Thatcher 1, M. Drost 2, T. K. Schalue 3, and R. M. Roberts 4

1 Department of Dairy and Poultry Sciences, University of Florida. Gainesville 32611-0920
2 Department of Large Animal Clinical Sciences, University of Florida, Gainesville 32611-0920
3 Department of Animal Science, University of Florida, Gainesville 32611
4 Department of Animal Sciences, University of Missouri, Columbia 65211

Endometrial oxytocin receptors and total production of PGF by endometrial epithelial cells were measured in 10 cyclic cows after intrauterine injections of recombinant bovine interferon-tau plus BSA or BSA alone. Cows received twice daily injections (via intrauterine catheters) of 200 µg of recombinant bovine interferon-tau plus 1.3 mg of BSA (n = 5) or 1.5 mg of BSA (n = 5) from d 14 to 17 after estrus. On d 17, the reproductive tracts of each cow was removed at slaughter, and endometrial epithelial cells were cultured with 0, 2, or 50 ng/ml of recombinant bovine interferon-tau. After 24 h, oxytocin (2 x 10-7 M) was added to one-half of the culture wells, and the medium was sampled at 0, 30, and 90 min for analysis of total PGF (PGF plus 13,14-dihydro-15-keto-PGF2alpha). In vivo treatment with recombinant bovine interferon-tau + BSA reduced total secretion of PGF in culture (1.49 ± 0.06 vs. 2.80 ± 0.07 ng/µg of DNA), but did not block the oxytocin-induced stimulation in total secretion of PGF. In vitro treatment of cells with recombinant-bovine interferon-tau did not decrease basal secretion of total PGF. Oxytocin receptor binding at d 17 was low in both treatments but slightly attenuated in the group treated with recombinant bovine interferon-tau.

Key Words: interferon-tau • oxytocin receptors • prostaglandin F • uterus

Submitted on July 28, 1995
Accepted on February 20, 1996




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