Toll-Like Receptor 4 Mediates the Response of Epithelial and Stromal Cells to Lipopolysaccharide in the Endometrium

Sheldon, I. Martin; Roberts, Mary Flynn

doi:10.1371/journal.pone.0012906

Cited by 76 publications

(71 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The interaction between LPS and TLR4 results in the activation of intracellular signaling through myeloid differentiation factor 88 (MyD88) and TIR-domain-containing adapter-inducing interferon-β (TRIF) pathways, leading to the activation of major mitogen-activated protein kinases (MAPKs) and translocation of nuclear transcription factor-κB (NF-κB) (Sheldon and Roberts, 2010;Kawai and Akira, 2011;Huang et al, 2016). NF-κB regulates the expression of cytokines, including interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α (TNF-α), which are essential mediators of the inflammation response (Wang et al, 2012;Liu et al, 2014;Huang et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Punicalagin protects bovine endometrial epithelial cells against lipopolysaccharide-induced inflammatory injury

Lyu

Chen

Wang

et al. 2017

J. Zhejiang Univ. Sci. B

View full text Add to dashboard Cite

Abstract:Objective: Bovine endometritis is one of the most common reproductive disorders in cattle. The aim of this study was to investigate the anti-inflammation potential of punicalagin in lipopolysaccharide (LPS)-induced bovine endometrial epithelial cells (bEECs) and to uncover the underlying mechanisms. Methods: bEECs were stimulated with different concentrations (1, 10, 30, 50, and 100 μg/ml) of LPS for 3, 6, 9, 12, and 18 h. MTT assay was used to assess cell viability and to identify the conditions for inflammatory injury and effective concentrations of punicalagin. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess gene expression of pro-inflammatory cytokines. Western blotting was used to assess levels of inflammation-related proteins. Results: Treatment of bEECs with 30 µg/ml LPS for 12 h induced cell injury and reduced cell viability. Punicalagin (5, 10, or 20 µg/ml) pretreatment significantly decreased LPS-induced productions of interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α (TNF-α) in bEECs. Molecular research showed that punicalagin inhibited the activation of the upstream mediator nuclear factor-κB (NF-κB) by suppressing the production of inhibitor κBα (IκBα) and phosphorylation of p65. Results also indicated that punicalagin can suppress the phosphorylation of mitogen-activated protein kinases (MAPKs) including p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK). Conclusions: Punicalagin may attenuate LPS-induced inflammatory injury and provide a potential option for the treatment of dairy cows with Escherichia coli endometritis.

show abstract

Section: Introductionmentioning

confidence: 99%

Punicalagin protects bovine endometrial epithelial cells against lipopolysaccharide-induced inflammatory injury

Lyu

Chen

Wang

et al. 2017

J. Zhejiang Univ. Sci. B

View full text Add to dashboard Cite

show abstract

“…Although some studies investigated the interactions between LPS and bovine endometrial cells (EECs) (Herath et al, 2009;Sheldon and Roberts, 2010), the signaling molecules of the TLR4 signaling pathway in bovine hepatocytes have not been well characterized.…”

Section: Discussionmentioning

confidence: 99%

Attenuated mRNA expression of lipid metabolism genes in primary hepatocytes following lipopolysaccharide treatment in dairy cows

Wang¹,

Li²,

Wang³

et al. 2015

Genet. Mol. Res.

View full text Add to dashboard Cite

ABSTRACT. The influence of ruminal acidosis on ruminal microbiology and metabolite production has received considerable attention, but little is known regarding the systemic manifestations that arise from ruminal acidosis. Lipopolysaccharide (LPS) is released in the gastrointestinal tract upon ingestion of high-grain or high-fat diets, and it has been implicated in the etiology of multiple energy-and lipid-related metabolic disturbances in ruminants. The liver plays a crucial role in the acute phase response to intruding pathogens. The effect of blood LPS in subacute ruminal acidosis on lipid metabolism in the liver has not been established. In this study, cell cultures were photographed using an inverted microscope. We observed that hepatocytes changed their morphologies from irregular triangle to circular (contraction) shapes; the number of contracted cells increased with the increasing LPS doses. This suggests that LPS can 3719 Lipid metabolism genes in primary hepatocytes ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 3718-3728 (2015) promote cell contraction and take off the wall, ultimately leading to cell apoptosis. With changes in LPS exposure, hepatocyte number also changes. We explored lipid metabolism in the liver using quantitative reverse transcription-polymerase chain reaction to detect the expression of key lipid metabolism enzymes in hepatocytes. We found that Toll-like receptor 4 signaling pathway mediated by LPS could attenuate mRNA expression of fatty acid synthesis genes and increase the expression of fatty acid transport genes in primary hepatocytes following LPS treatment in dairy cows.

show abstract

“…We concluded that altered expression and production of pro-inflammatory cytokines postpartum could contribute to impaired inflammatory response and predispose cows to development of metritis. (52). They created mutant mice lacking TLR4 and showed that intrauterine infusion of purified LPS induced an inflammatory response with accumulation of granulocytes throughout the endometrium of wild type (WT) but not Tlr4(-/-) mice.…”

Section: Mechanism Of Recognition Of Pathogens By Professional Phagocmentioning

confidence: 99%

Recent advances in the immunology and uterine microbiology of healthy cows and cows that develop uterine disease

Galvão¹,

Santos²

2014

Turk J Vet Anim Sci

View full text Add to dashboard Cite

Uterine diseases are highly prevalent in dairy cows. Causes of uterine diseases are multifactorial. There is good evidence for the susceptibility of the host and for the role of pathogenic bacteria, and less evidence for the effect of the environment. Uterine and leukocyte immune response is impaired early postpartum in cows that develop uterine disease. The decrease in immune function is associated with a decrease in calcium postpartum and an increase in NEFA and BHBA. Both endometrial cells and granulosal cells possess toll-like receptors (TLR) that can recognize and mount an inflammatory response to pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharides (LPSs) or lipopeptides. Exposure to LPSs leads to endocrine dysregulation, which may affect steroidogenesis, ovulation and luteolysis. Some E. coli possess specific virulence factors such as fimH, hlyA, cdt, kpsMII, ibeA, and astA that cause uterine disease in dairy cows. These E. coli are associated with the occurrence of other pathogenic bacteria such as A. pyogenes, F. necrophorum, and Bacteroides spp., which act synergistically to cause uterine disease. The combined effect of bacterial infection and activation of inflammation is damage to the endometrium and embryo, delayed ovulation, shortened or extended luteal phase, and decreased fertility.

show abstract

Toll-Like Receptor 4 Mediates the Response of Epithelial and Stromal Cells to Lipopolysaccharide in the Endometrium

Cited by 76 publications

References 34 publications

Punicalagin protects bovine endometrial epithelial cells against lipopolysaccharide-induced inflammatory injury

Punicalagin protects bovine endometrial epithelial cells against lipopolysaccharide-induced inflammatory injury

Attenuated mRNA expression of lipid metabolism genes in primary hepatocytes following lipopolysaccharide treatment in dairy cows

Recent advances in the immunology and uterine microbiology of healthy cows and cows that develop uterine disease

Contact Info

Product

Resources

About