title: Effects of lipopolysaccharide (LPS) and peptidoglycan (PGN) on estradiol production in bovine granulosa cells from small and large follicles.
abstract: In cows, postpartum uterine infection due to bacteria that produce lipopolysaccharide (LPS) or peptidoglycan (PGN) leads to ovarian dysfunction. The aim of this study was to determine the effect of LPS and/or PGN on estradiol production from granulosa cells from small and large follicles in the bovine ovary. Granulosa cells from small and large ovarian follicles were exposed to LPS and/or PGN in vitro. LPS inhibited the expression of TLR4, CD14, MD2 and NOD1 genes in FSH-treated granulosa cells from small follicles. LPS suppressed estradiol (E2) production in granulosa cells from small and large follicles, while PGN inhibited E2 production in granulosa cells from large follicles. LPS or PGN did not affect granulosa cell survival. Although LPS alone suppressed E2 production in granulosa cells from small and large follicles, E2 production was not further suppressed when PGN was added to culture medium with LPS alone. Our data demonstrated that susceptibility to LPS or PGN in granulosa cells depends on the follicle developmental stage. The results of the present study suggest that ovarian dysfunction in cows with postpartum uterine infection may be caused by inhibitory effects of LPS and PGN on E2 production in granulosa cells.
authors: Graduate School of Animal and Food Hygiene, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Hokkaido 080-8555, Japan. shimizut@obihiro.ac.jp
authors: T
authors: T
authors: Shimizu
authors: K
authors: K
authors: Miyauchi
authors: K
authors: K
authors: Shirasuna
authors: H
authors: H
authors: Bollwein
authors: F
authors: F
authors: Magata
authors: C
authors: C
authors: Murayama
authors: A
authors: A
authors: Miyamoto
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000276:immunology / Q000473:pathology / Q000662:veterinary; D002417:Cattle; D002418:Cattle Diseases / Q000276:immunology / Q000473:pathology; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004359:Drug Therapy, Combination; D004958:Estradiol / Q000378:metabolism*; D005260:Female; D005640:Follicle Stimulating Hormone / Q000494:pharmacology; D015870:Gene Expression / Q000187:drug effects; D006107:Granulosa Cells / Q000187:drug effects* / Q000378:metabolism; D018950:Lipopolysaccharide Receptors / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D051218:Lymphocyte Antigen 96 / Q000235:genetics / Q000378:metabolism; D053474:Nod1 Signaling Adaptor Protein / Q000235:genetics / Q000378:metabolism; D006080:Ovarian Follicle / Q000166:cytology* / Q000502:physiology; D010457:Peptidoglycan / Q000494:pharmacology*; D049590:Postpartum Period; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism; D014591:Uterine Diseases / Q000276:immunology / Q000473:pathology / Q000662:veterinary; D014599:Uterus / Q000187:drug effects / Q000473:pathology
chemical_list: D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D051218:Lymphocyte Antigen 96; D053474:Nod1 Signaling Adaptor Protein; D010457:Peptidoglycan; D051197:Toll-Like Receptor 4; D004958:Estradiol; D005640:Follicle Stimulating Hormone