Lipopolysaccharide-induced mechanisms of ovarian dysfunction in cows with uterine inflammatory diseases

Abstract

Uterine inflammatory diseases commonly occur in postpartum dairy cows, resulting in reduced reproductive performance due to aberrant uterine and ovarian activity. Infection of the uterus with gram-negative bacteria results in the detection of lipopolysaccharide (LPS) in the plasma and follicular fluid of cows along with uterine inflammation. LPS acts on follicular components such as theca cells, granulosa cells, and follicle-enclosed oocytes, leading to impaired follicular activity. Follicles with a high LPS environment exhibit reduced follicular steroidogenesis due to the inhibition of steroidogenic enzyme transcription. Primary cell cultures of bovine granulosa and theca cells have shown that LPS acts on follicular cells to impair steroid production, which may disturb follicle growth and/or reduce their ability to ovulate. Even if ovulation occurs, cows with uterine inflammation are less likely to conceive because in addition to uterine damage, LPS also impairs the developmental competence of oocytes. LPS perturbs the nuclear and cytoplasmic maturation of bovine oocytes. Moreover, oocytes matured in an LPS treatment are less likely to develop into the blastocyst stage. Such oocytes also have a reduced number of trophoblast cells in blastocysts. Therefore, the detrimental effects of LPS on ovarian activity may be partly responsible for infertility in cows with uterine inflammation. Novel treatment and prevention strategies for uterine inflammatory diseases can be developed by advancing our knowledge of the pathophysiology underlying ovarian dysfunction, and this can only be achieved by further research. The present review outlines the molecular pathogenesis of LPS-induced ovarian dysfunction.

Effects of LPS on the Secretion of Gonadotrophin Hormones and Expression of Genes in the Hypothalamus-Pituitary-Ovary (HPG) Axis in Laying Yangzhou Geese

“…However, the mRNA expression of FSHR and LHR in both the GLs and TLs of hierarchical follicles was significantly decreased, and LPS may suppress the stimulatory effects of gonadotrophin hormones on ovarian steroidogenesis by decreasing the expression of gonadotropin receptors. In bovines, the FSHR and LHR mRNA abundance in F1 and F2 higher follicle fluids LPS concentrations was significantly reduced and was accompanied by altered E2 and P4 in follicle fluids [40]. The results indicated that LPS may exert the same effects on FSHR and LHR gene expression in mammals and birds.…”

Zinc-nanoparticles alleviate the ovarian damage induced by bacterial lipopolysaccharide (LPS) in pregnant rats and their fetuses

“… 2019 ; Lv et al. 2021 ), the ovaries and uteruses of cows (Magata 2020 ), the uteruses of mice (Jaiswal et al. 2009 ; Wolfson et al.…”

“… 2001 ). Magata added that LPS exposure during gestation results in reduced mitochondrial membrane potential in mature oocytes and consequently leads to follicular damage (Magata 2020 ). The histopathological alterations in the uterus of LPS-treated rats were recently explained by Lu et al., who reported that LPS exposure during gestation can induce glandular and epithelial damage of the uterine endometrium via inactivation of E-cadherin expression (Lu et al.…”

Superoxide Dismutase Expression in the Ovaries of Periodontitis Animal Models Induced by Porphyromonas gingivalis and Treated with Cassava Leaves Extract

“…Lipopolysaccharide as a virulence factor of P. gingivalis might induce inflammation and apoptosis of granulosa cells [19]. Several studies suggested that bacteria enhanced reactive oxygen species (ROS) production and oxidative stress, which induced folliculogenesis alteration [18,20,21].…”