Lipopolysaccharide (LPS)-induced inflammation alters expression of TGF beta signaling components in the bovine...

Lipopolysaccharide (LPS)-induced inflammation resulting from postpartum bacterial infections is a major cause of reduced fertility in cattle; however, its effects on oviductal function remain poorly understood. This study investigated the impact of LPS on the expression of inflammatory and TGFβ/BMP signaling components in bovine oviductal epithelial cells (BOEC) under hormonally defined conditions mimicking the follicular and luteal phases of the estrous cycle. Cytotoxicity analyses revealed that BOEC derived from short-term oviductal tissue explants cultures were significantly more resistant to LPS exposure than cells from conventional monolayer cultures, even at LPS concentrations that severely compromised the viability of primary epithelial and stromal cells in monolayer. Gene expression analysis of inflammatory mediators (IL6, TNFA, NFKB1, IL10) and TGFβ/BMP signaling components (TGFB1, BMP7, ID3) demonstrated that the hormonal environment modulates epithelial responses to LPS. In hormone-free conditions, LPS upregulated pro-inflammatory genes along with TGFB1, BMP7, and ID3. Under follicular-like conditions, LPS upregulated IL10, TGFB1 and BMP7 mRNAs. In luteal-like conditions, LPS downregulated pro-inflammatory IL6, TNFA, and NFKB1 transcripts while upregulating IL10 and TGFB/BMP-associated transcripts, consistent with hormone-dependent activation of regulatory and repair-related pathways. Epithelial functionality assessed through adhesion to collagen matrices showed that LPS compromised BOEC adhesion and that this reduction was differentially affectedd by ovarian steroids. These findings suggest that the bovine oviductal immune response to inflammation is regulated by both the hormonal context and tissue organization, with TGFβ/BMP signaling emerging as a potential key axis contributing to epithelial homeostasis, which may have implications for reproductive function in cattle.