LPS-induces IL-6 and IL-8 gene expression in bovine endometrial cells “through DNA methylation”

Wang, Jun; Yan, Xiaoxiao; Nesengani, Lucky T.; He, Ding; Yang, Lei; Lu, Wenjing

doi:10.1016/j.gene.2018.07.074

Cited by 24 publications

(8 citation statements)

References 24 publications

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“…IL-1β, IL-6, and TNF-α play an important role in the development of endometritis during the early postpartum period (Brodzki et al, 2015). CXCL8 and CXCL5 are cytokines belonging to the chemokine family (Wang et al, 2018). The upregulation of pro-inflammatory mediators, including CXCL8, IL-1β, and IL-6, is involved in the pathogenesis of bacterial infection (Angrisano et al, 2010).…”

Section: Fig 7 Effect Of Catalpol On Endometrial Inflammation Of Lpsmentioning

confidence: 99%

Catalpol ameliorates LPS-induced endometritis by inhibiting inflammation and TLR4/NF-κB signaling

Zhang

Yang

et al. 2019

J. Zhejiang Univ. Sci. B

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Catalpol is the main active ingredient of an extract from Radix rehmanniae, which in a previous study showed a protective effect against various types of tissue injury. However, a protective effect of catalpol on uterine inflammation has not been reported. In this study, to investigate the protective mechanism of catalpol on lipopolysaccharide (LPS)-induced bovine endometrial epithelial cells (bEECs) and mouse endometritis, in vitro and in vivo inflammation models were established. The Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway and its downstream inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qRT-PCR), western blot (WB), and immunofluorescence techniques. The results from ELISA and qRT-PCR showed that catalpol dose-dependently reduced the expression of pro-inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin (IL)-1β, and IL-6, and chemokines such as C-X-C motif chemokine ligand 8 (CXCL8) and CXCL5, both in bEECs and in uterine tissue. From the experimental results of WB, qRT-PCR, and immunofluorescence, the expression of TLR4 and the phosphorylation of NF-κB p65 were markedly inhibited by catalpol compared with the LPS group. The inflammatory damage to the mouse uterus caused by LPS was greatly reduced and was accompanied by a decline in myeloperoxidase (MPO) activity. The results of this study suggest that catalpol can exert an anti-inflammatory impact on LPS-induced bEECs and mouse endometritis by inhibiting inflammation and activation of the TLR4/NF-κB signaling pathway.

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Section: Fig 7 Effect Of Catalpol On Endometrial Inflammation Of Lpsmentioning

confidence: 99%

Catalpol ameliorates LPS-induced endometritis by inhibiting inflammation and TLR4/NF-κB signaling

Zhang

Yang

et al. 2019

J. Zhejiang Univ. Sci. B

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“…Recent study demonstrated that LPS promoted the production of IL-1β and TNF-α in response to infection mediated by a mechanism for A2AR targeting in microglia [29]. LPS-stimulated IL-6 and IL-8 mRNA expression by IL-6 and IL-8 promoter methylation is crucial for the inflammatory response in bovine endometrial cells [30]. These studies indicated that LPS could stimulated altered inflammatory factors mediated by various mechanisms in diverse cell types and further illustrated that individual functions of TCs on various cell types.…”

Section: Discussionmentioning

confidence: 99%

Telocytes inhibited inflammatory factor expression and enhanced cell migration in LPS-induced skin wound healing models in vitro and in vivo

et al. 2020

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Background: Cell proliferation and death are key components of wound healing and tissue repair. Telocytes (TCs) represent a newly discovered cell type that can protect tissue from acute injury via cell-cell communication with adjacent cells. The aim of this study was to use a mouse model of skin wound healing and lipopolysaccharide (LPS)induced cell injury to evaluate the effects of TCs on skin wound healing in vivo and in vitro. Material/methods: Immunohistochemical staining was performed to evaluate the alteration of TCs in tissues from normal and chronic wound patients. Then, a male C57BL/6 mouse wound model of the back was established. The mice were divided randomly into three groups, and wound healing was estimated according to the wound healing rate and histology. An LPS-induced co-culture model of a mouse lung telocyte cell line (TCs) with human keratinocyte (HaCaT), human dermal microvascular endothelial cell (HDMEC) or murine fibroblast (L929) cell lines was established to analyse the effects of TCs on constitutive cell types of the skin. Cell proliferation, migration and apoptosis were examined, and reactive oxygen species (ROS) and inflammatory factors in HaCaT cells, HDMECs, and L929 cells were detected to study the mechanisms involved in TC protection in skin wounds. Results: TCs were significantly increased in tissues from chronic wound patients compared with healthy controls. Wound healing was significantly improved in wound mouse models treated with exogenous TCs compared with LPSinduced models. TCs reversed the LPS-induced inhibition of HaCaT cells and HDMECs and reduced the LPS-induced apoptosis of HaCaT cells and the death ratios of HDMECs and L929 cells. TCs reversed LPS-induced ROS in HDMECs and L929 cells and decreased inflammatory factor mRNA levels in HaCaT cells, HDMECs and L929 cells. Conclusions: TCs reduce wound healing delay, and inflammatory responses caused by LPS might be mediated by inflammatory inhibition, thus restricting apoptosis and promoting migration of the main component cell types in the skin.

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“…CXCL1 and IL-8 are representative inflammatory cytokines in endometrial cells exposed to LPS. IL-8 and CXCL1 are cytokines with neutrophil chemotactic and activating activity and T cell chemotactic activity that play a major role in the recruitment of leukocytes to the endometrium via the CXCR1 and CXCR2 pathways [46][47][48]. However, the relationship between IL-33 and LPS in endometrial epithelial cells remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Detrimental effects of lipopolysaccharide on the attachment and outgrowth of various trophoblastic spheroids on human endometrial epithelial cells

Kim

Choi

Yoon

et al. 2021

Clin Exp Reprod Med

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Objective: Lipopolysaccharide (LPS) from Gram-negative bacteria causes poor uterine receptivity by inducing excessive inflammation at the maternal-fetal interface. This study aimed to investigate the detrimental effects of LPS on the attachment and outgrowth of various types of trophoblastic spheroids on endometrial epithelial cells (ECC-1 cells) in an in vitro model of implantation.Methods: Three types of spheroids with JAr, JEG-3, and JAr mixed JEG-3 (JmJ) cells were used to evaluate the effect of LPS on early implantation events. ECC-1 cells were treated with LPS to mimic endometrial infection, and the expression of inflammatory cytokines and adhesion molecules was analyzed by quantitative real-time polymerase chain reaction and western blotting. The attachment rates and outgrowth areas were evaluated in the various trophoblastic spheroids and ECC-1 cells treated with LPS.Results: LPS treatment significantly increased the mRNA expression of inflammatory cytokines (CXCL1, IL-8, and IL-33) and decreased the protein expression of adhesion molecules (ITGβ3 and ITGβ5) in ECC-1 cells. The attachment rates of JAr and JmJ spheroids on ECC-1 cells significantly decreased after treating the ECC-1 cells with 1 and 10 μg/mL LPS. In the outgrowth assay, JAr spheroids did not show any outgrowth areas. However, the outgrowth areas of JEG-3 spheroids were similar regardless of LPS treatment. LPS treatment of JmJ spheroids significantly decreased the outgrowth area after 72 hours of coincubation.Conclusion: An in vitro implantation model using novel JmJ spheroids was established, and the inhibitory effects of LPS on ECC-1 endometrial epithelial cells were confirmed in the early implantation process.

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LPS-induces IL-6 and IL-8 gene expression in bovine endometrial cells “through DNA methylation”

Cited by 24 publications

References 24 publications

Catalpol ameliorates LPS-induced endometritis by inhibiting inflammation and TLR4/NF-κB signaling

Catalpol ameliorates LPS-induced endometritis by inhibiting inflammation and TLR4/NF-κB signaling

Telocytes inhibited inflammatory factor expression and enhanced cell migration in LPS-induced skin wound healing models in vitro and in vivo

Detrimental effects of lipopolysaccharide on the attachment and outgrowth of various trophoblastic spheroids on human endometrial epithelial cells

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