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Staphylococcus aureus-Induced Necroptosis Promotes Mitochondrial Damage in Goat Endometrial Epithelial Cells.

ABSTRACT: Endometrial cell death is induced by bacterial infection, resulting in damage to the physical barriers and immune function. An in-depth understanding of the mechanisms of endometrial epithelial cell necroptosis might provide new insights into the treatment of uterine diseases. In the present study, we investigated the effect of Staphylococcus aureus on goat endometrial epithelial cell (gEEC) necroptosis, and the underlying molecular mechanism. We found that S. aureus induced significant necroptosis in gEECs by increasing the expression of key proteins of the RIPK1/RIPK3/MLKL axis; importantly, this effect was alleviated by inhibitors of RIPK1, RIPK3, and MLKL. Moreover, we found that the main triggers of gEEC necroptosis induced by S. aureus were not the toll-like receptors (TLRs) and tumor necrosis factor receptor (TNFR), but membrane disruption and ion imbalance. Moreover, we observed a significant decrease in the mitochondrial membrane potential, indicating mitochondrial damage, in addition to increased cytochrome c levels and reactive oxygen species (ROS) generation in S. aureus-infected gEECs; these, effects were also suppressed by the inhibitors of RIPK1, RIPK3, and MLKL. Taken together, these data revealed the molecular mechanism of S. aureus-induced gEEC necroptosis and provided potential new targeted therapies for clinical intervention in bacterial infections.

SUBMITTER: Yi Y

PROVIDER: S-EPMC9454985 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature

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Staphylococcus aureus-Induced Necroptosis Promotes Mitochondrial Damage in Goat Endometrial Epithelial Cells.

Yi Yanyan Y Gao Kangkang K Lin Pengfei P Chen Huatao H Zhou Dong D Tang Keqiong K Wang Aihua A Jin Yaping Y

Animals : an open access journal from MDPI 20220829 17

Endometrial cell death is induced by bacterial infection, resulting in damage to the physical barriers and immune function. An in-depth understanding of the mechanisms of endometrial epithelial cell necroptosis might provide new insights into the treatment of uterine diseases. In the present study, we investigated the effect of Staphylococcus aureus on goat endometrial epithelial cell (gEEC) necroptosis, and the underlying molecular mechanism. We found that S. aureus induced signif ...[more]

PMID: 36077938

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Project description:ObjectiveRutin, also called vitamin P, is a flavonoids from plants. Previous studies have indicated that rutin can alleviate the injury of tissues and cells by inhibiting oxidative stress and ameliorating inflammation. There is no report on the protective effects of rutin on goat rumen epithelial cells (GRECs) at present. Hence, we investigated whether rutin can alleviate lipopolysaccharide (LPS)-induced damage in GRECs.MethodsGRECs were cultured in basal medium or basal medium containing 1 μg/mL LPS, or 1 μg/mL LPS and 20 μg/mL rutin. Six replicates were performed for each group. After 3-h culture, the GRECs were harvested to detect the relevant parameters.ResultsRutin significantly enhanced the cell activity (p<0.05) and transepithelial electrical resistance (TEER) (p<0.01) and significantly reduced the apoptosis rate (p<0.05) of LPSinduced GRECs. Rutin significantly increased superoxide dismutase, glutathione peroxidase, and catalase activity (p<0.01) and significantly decreased lactate dehydrogenase activity and reactive oxygen species and malondialdehyde (MDA) levels in LPS-induced GRECs (p<0.01). The mRNA and protein levels of interleukin 6 (IL-6), IL-1β, and C-X-C motif chemokine ligand 8 (CXCL8) and the mRNA level of tumor necrosis factor-α (TNF-α) and chemokine C-C motif ligand 5 (CCL5) were significantly increased in LPS-induced GRECs (p<0.05 or p<0.01), while rutin supplementation significantly decreased the mRNA and protein levels of IL-6, TNF-α, and CXCL8 in LPS-induced GRECs (p<0.05 or p<0.01). The mRNA level of toll-like receptor 2 (TLR2), and the mRNA and protein levels of TLR4 and nuclear factor κB (NF-κB) was significantly improved in LPS-induced GRECs (p<0.05 or p<0.01), whereas rutin supplementation could significantly reduce the mRNA and protein levels of TLR4 (p<0.05 or p<0.01). In addition, rutin had a tendency of decreasing the protein levels of CXCL6, NF-κB, and inhibitor of nuclear factor kappa-B alpha (0.05< p<0.10). Rutin could significantly decreased interferon regulatory factor 3 mRNA expression in LPS-induced GRECs (p<0.05), whereas interferon induced protein with tetratricopeptide repeats 3 (IFIT3) and toll-interacting protein (TOLLIP) mRNA expression was not significantly different between the groups. LPS reduced the tight junction protein zonula occludin 1 (ZO-1) level in GRECs whereas rutin enhanced it. Rutin significantly improved tight junction protein Claudin-1 mRNA expression in LPS-induced GRECs (p<0.01), but could not affect tight junction protein Occludin mRNA expression.ConclusionRutin alleviated LPS-induced barrier damage in GRECs by improving oxidation resistance and anti-inflammatory activity, which may be related to TLR/NF-κB signaling pathway inhibition.

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Staphylococcus aureus-Induced Necroptosis Promotes Mitochondrial Damage in Goat Endometrial Epithelial Cells.

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<i>Staphylococcus aureus</i>-Induced Necroptosis Promotes Mitochondrial Damage in Goat Endometrial Epithelial Cells.

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