Lipopolysaccharide increases Toll-like receptor 4 and downstream Toll-like receptor signaling molecules expression in bovine endometrial epithelial cells

Fu, Yunhe; Liu, Bo; Feng, Xiaowei; Liu, Zhicheng; Liang, Dakai; Li, Fengyang; Li, Depeng; Cao, Yongguo; Feng, Shuang; Zhang, Xichen; Zhang, Naisheng; Yang, Zhengtao

doi:10.1016/j.vetimm.2012.09.039

Cited by 56 publications

(67 citation statements)

References 32 publications

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“…LPS, a cell wall component of Gram-negative bacteria, is a well-known inducer of inflammation, and exposure of cells to LPS has been shown to promote the release of pro-inflammatory cytokines (Lim et al, 2012;Fu et al, 2013;Wang et al, 2013), making LPS a good stimulant of inflammation. In many previous reports, the concentrations of LPS used in vitro were less than 1 µg/ml (Choi et al, 2007;Wang et al, 2012;Qi et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

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

Lyu

Chen

Wang

et al. 2017

J. Zhejiang Univ. Sci. B

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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.

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Section: Discussionmentioning

confidence: 99%

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

Lyu

Chen

Wang

et al. 2017

J. Zhejiang Univ. Sci. B

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“…However, expression of both TLR2 and TLR4 mRNA increased in bovine mammary (Ibeagha-Awemu et al 2008, Ma et al 2011 and endometrial epithelial cells (Fu et al 2013) stimulated with LPS. Furthermore, these studies indicate that TLR4 is present on cells other than leukocytes.…”

Section: Introductionmentioning

confidence: 98%

“…In cows, TLR4 mRNA and protein were detected in endometrial stromal and epithelial cells by RT-PCR and flow cytometry (Herath et al 2006). Activation of TLRs by LPS was observed in endometrial (Fu et al 2013) as well as in mammary epithelial cells (Ibeagha-Awemu et al 2008), thus inducing the downstream signaling cascade that culminates in the secretion of proinflammatory cytokines. In bovine granulosa cells, TLR4 was detected and an inflammatory response to LPS was observed and linked to reduced fertility, due to reduced follicular steroidogenesis .…”

Section: Introductionmentioning

confidence: 99%

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

Lüttgenau¹,

Herzog²,

Strüve³

et al. 2016

Reproduction

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When given intravenously (iv), lipopolysaccharide (LPS) transiently suppresses the structure and function of the bovine corpus luteum (CL). This is associated with increased release of prostaglandin (PG) F 2a metabolite. The underlying regulatory mechanisms of this process remain, however, obscure. Therefore, the aims of this study were: i) to investigate the expression of the LPS receptor toll-like receptor 4 (TLR4) and 2 (TLR2) in the bovine CL during early, mid-and late luteal phases; and ii) to further dissect the mechanisms of LPS-mediated suppression of luteal function. As revealed by semi-quantitative qPCR and immunohistochemistry, both receptors were detectable throughout the luteal lifespan. Their mRNA levels increased from the early toward the mid-luteal phase; no further changes were observed thereafter. The TLR4 protein seemed more highly represented than TLR2. The cellular localization of TLRs was in blood vessels; weaker signals were observed in luteal cells. Additionally, cows were treated either with LPS (iv, 0.5 mg/kg BW) or with saline on Day 10 after ovulation. Samples were collected 1200 h after treatment and on Day 10 of the respective subsequent (untreated) cycle. The mRNA expression of several possible regulatory factors was investigated, revealing the suppression of PGF 2a receptor (PTGFR), STAR protein and 3b-hydroxysteroid dehydrogenase, compared with controls and subsequent cycles. The expression of TLR2 and TLR4, interleukin 1a (IL1A) and 1b (IL1B) and of PGF 2a and PGE 2 synthases (HSD20A and mPTGES respectively) was increased. The results demonstrate the presence of TLR2 and TLR4 in the bovine CL, and implicate their possible involvement in the deleterious effects of LPS on its function.

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“…Herath et al (2009) and Fu et al (2013) also found that expression of TLR4 was up-regulated when bovine EECs were stimulated by LPS. The results showed that the adapter molecule MyD88, transcription factor NF-kB and cytokine TNF-a, IL-1, IL-6, and IL-8 were up-regulated when bovine EECs were challenged with LPS (Fu et al, 2013).…”

Section: Discussionmentioning

confidence: 89%

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.

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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.

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Lipopolysaccharide increases Toll-like receptor 4 and downstream Toll-like receptor signaling molecules expression in bovine endometrial epithelial cells

Cited by 56 publications

References 32 publications

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

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

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

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

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