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Investigates glucocorticoid role in inflammatory responses in bovine oviduct epithelial cells, indicating potential therapeutic strategies.
The bovine oviduct supports early reproductive events that require a balance between immune defense and tolerance. Glucocorticoids are well-known immune modulators; however, their presence, regulation, and functional relevance in the bovine oviduct remain poorly understood. This study investigated the presence and role of the corticosteroid system in the bovine oviduct and cultured bovine oviduct epithelial cells (BOECs). Bovine oviducts were collected during estrous cycle, fixed in 4% paraformaldehyde and processed for immunohistochemistry. BOECs were harvested from the ampulla and isthmus and cultured under sequential progesterone and estradiol treatment to mimic estrous cycles. On day 8, which equivalent to post‑ovulation day 1 in vivo, cells were treated with lipopolysaccharide (LPS; 1 μg/ml), cortisol (100 nM), cortisone (100 nM), or their combinations for 24 h. After culture, cells were harvested for gene analysis by RT-PCR, while spent media were collected for cortisol measurement by ELISA. Immunohistochemistry revealed predominant epithelial localization of NR3C1, NR3C2, HSD11B1, and HSD11B2 in both ampulla and isthmus. During 7-day preculture, expression of NR3C1 and HSD11B1 persisted, whereas that of NR3C2 and HSD11B2 declined sharply. LPS treatment on day 8 sharply upregulated TLR2, TNF, IL1B, IL6, CXCL8 and HSD11B1, whereas the concomitant treatment with cortisol suppressed all LPS-induced cytokines. BOECs were capable to convert added cortisone to cortisol, and LPS doubled this through up-regulating HSD11B1. Locally produced cortisol also suppressed LPS-induced cytokines. Collectively, these findings demonstrate that BOECs possess a functional glucocorticoid system, capable of producing cortisol from cortisone, which in turn suppresses LPS-induced inflammation.
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ADEMOLA et al. (2026) studied this question.
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