Lipopolysaccharide (LPS) Inhibits Steroid Production in Theca Cells of Bovine Follicles <i>In Vitro</i>: Distinct Effect of LPS on Theca Cell Function in Pre- and Post-selection Follicles

Abstract

In postpartum dairy cows, lipopolysaccharide (LPS) derived from gram-negative bacteria such as Escherichia coli causes uterine inflammation and leads to ovarian dysfunction. The aim of this study was to determine the effect of LPS on steroid production in bovine theca cells at different stages of follicular development. Theca cells isolated from pre- and post-selection follicles (PRFs, <8.5 mm in diameter, and POFs, >8.5 mm in diameter, respectively) of bovine ovaries were exposed to LPS under luteinizing hormone (LH) conditions, estradiol (E2) conditions or both conditions in vitro. Bovine theca cells expressed the LPS receptor gene complex: Toll-like receptor 4 (TLR4), CD14 and MD2. LPS suppressed progesterone (P4) and androstenedione (A4) production with downregulation of steroidogenic enzyme transcripts when theca cells were stimulated with LH. By contrast, LPS did not affect P4 or A4 production when theca cells were stimulated with E2. P4 and A4 production in theca cells from PRFs was suppressed by LPS as early as at 48 h of culture, whereas the effect of LPS on theca cells from POFs was observed at 96 h of culture. The results demonstrate that LPS inhibits steroid production in theca cells under LH conditions. Moreover, theca cells from POFs showed a slower response to LPS compared with that of theca cells from PRFs, which might imply a distinct effect of LPS on follicles at different developmental stages. These findings suggest a possible mechanism of ovarian dysfunction and subsequent infertility in cows with endometritis.

LPS-mediated effects and spatio-temporal expression of TLR2 and TLR4 in the bovine corpus luteum

“…Therefore, effects of LPS on the bovine CL do not seem to be restricted to TLRbearing immune cells that are normally present in luteal tissue as reported in a review by Walusimbi & Pate (2013). The localization of TLR4 in luteal cells was consistent with previous reports that established the presence of TLR4 in granulosa , Price & Sheldon 2013) and theca cells (Magata et al 2014) from ovarian follicles, which are the progenitors of the large and small luteal cells respectively (Alila & Hansel 1984).…”

Symposium review: Mechanisms of disruption of fertility by infectious diseases of the reproductive tract

“…Although LPS in follicular fluid may detrimentally affect oocytes (Magata and Shimizu, 2017), it is not yet understood whether LPS affects oocyte competence if the exposure occurs in preantral stages of development. It seems plausible, but remains to be shown, that granulosa and theca cells, known to express TLR (Herath et al, 2007;Magata et al, 2014b;Gu et al, 2016) respond to LPS (and indeed other PAMP) 3761 in earlier stages of development, potentially disrupting the intricate communication between oocyte and cumulus cells that is necessary for competent oocyte development.…”

Relationship between endometritis and oxidative stress in the follicular fluid and luteal function in the buffalo

“…The suppression of E 2 production by LPS is associated with downregulation of aromatase transcripts in the granulosa cells (Herath et al., ). High concentration of P 4 in the follicular fluid might be due to a decreased expression of 17α hydroxylase/17, 20‐lyase (CYP17) in the theca cells, which impairs the conversion of P 4 to androstenedione (Magata, Horiuchi, Miyamoto, & Shimizu, ). Pande et al.…”