In the dairy cow, puerperal uterine intra-luminal concentrations of PGE(2) are related to the establishment and severity of uterine infections. Here we evaluated whether the blood concentrations of PGE(2) and the gene transcription profiles of enzymes involved in its synthesis (cyclooxygenase-2 and prostaglandin E synthase) could be used as markers of predisposition and/or presence of puerperal uterine infections. We also studied the relationship between the endocrine status and the leukocyte profiles around parturition and the transcription patterns of the genes. Finally, we have characterized the in vitro gene transcription and expression response to a challenge of LPS. Gene transcription profiles, quantified by real-time PCR, were similar in normal puerperium and metritis/endometritis cows, indicating that they are not suitable markers of predisposition to/presence of puerperal uterine infections. Transcription decreased from 2 weeks before parturition until parturition, when a minimum was attained, and then increased during the first week postpartum. The lowest gene transcription, at parturition, was coincidental with the highest total leukocytes, polymorphonuclear neutrophils and CD14 positive cell numbers. It is suggested that by this mechanism, a large number of PMN can be recruited into the uterus after parturition, avoiding an excessive acute inflammatory response. The lowest gene transcription was also coincidental with the surge in cortisol concentrations, indicating that this hormone plays a main immunomodulatory role around parturition. Gene transcription was significantly greater after stimulation with LPS than in non-stimulated blood. We suggest that this PGE(2) producing cells might arrive to the uterine lumen, contributing to the local PGE(2) concentrations and mediating the inflammatory response.