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Increased circulating lipopolysaccharide (LPS) results from heat stress (HS) and bacterial infection, both of which are associated with reduced female fertility. Specific effects of low-level, repeated LPS exposure on the ovary are unclear, as many studies utilize a bolus model and/or high dosage paradigm. To better understand the effects of chronic LPS exposure on ovarian signaling and function, post-pubertal gilts (n = 20) were orally administered altrenogest for 14 d to synchronize the beginning of the follicular phase of the ovarian cycle. For 5 d after synchronization, gilts (163 ± 3 kg) received IV administration of LPS (0.1 µg/kg BW, n = 10) or saline (CT, n = 10) 4× daily. Blood samples were obtained on days 1, 3, and 5 of LPS treatment. Follicular fluid was aspirated from dominant follicles on day 5, and whole ovarian homogenate was used for transcript and protein abundance analysis via quantitative real-time PCR and western blotting, respectively. There were no treatment differences detected in rectal temperature on any day (P ≥ 0.5). Administering LPS increased plasma insulin (P &lt; 0.01), LPS-binding protein (LBP; P &lt; 0.01), and glucose (P = 0.08) on day 1, but no treatment differences thereafter were observed (P = 0.66). There were no treatment differences in follicular fluid concentration of LBP or 17β-estradiol (P = 0.42). Gilts treated with LPS had increased abundance of ovarian TLR4 protein (P = 0.01), but protein kinase B (AKT) and phosphorylated AKT (pAKT) were unchanged and no effect of LPS on components of the phosphatidylinositol 3 kinase (PI3K) pathway were observed. There was no impact of LPS on ovarian abundance of STAR or CYP19A1, nor ESR1, LDLR, CYP19A1, CYP17A1, or 3BHSD. In conclusion, repeated, low-level LPS administration alters inflammatory but not steroidogenic or PI3K signaling in follicular phase gilt ovaries.

Impact of repeated lipopolysaccharide administration on ovarian signaling during the follicular phase of the estrous cycle in post-pubertal pigs