Lipopolysaccharide-induced increases in porcine serum cortisol and progesterone concentrations are not mediated solely by prostaglandin F2 alpha.

The increase in steroid hormone blood levels in response to bacterial lipopolysaccharide (LPS) appears to be an important mechanism by which mammalian species regulate inflammation. This study examined changes in serum concentrations of cortisol, progesterone, and 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) in diestrous pigs following the intravenous injection of LPS and determined whether indomethacin would attenuate these changes. Serum cortisol and progesterone concentrations increased (P < 0.05) within 30 min after the administration of LPS, and the increases in steroid hormones were accompanied by a sharp, transient increase (P < 0.05) in PGFM levels. In the presence of indomethacin, serum PGFM levels did not change (P > 0.05); however, LPS enhanced (P < 0.05) cortisol and progesterone concentrations, although the increases were delayed. Serum concentrations of cortisol acutely increased (P < 0.05) immediately following both infusions of indomethacin. In summary, cortisol and progesterone concentrations increased irrespective of serum PGFM concentrations, thereby indicating that prostaglandin F2 alpha was not the sole mediator of LPS-induced changes in cortisol and progesterone concentrations.