Abstract
Simple SummaryThe toxicity mechanism of Staphylococcus aureus on goat endometrial epithelial cells (gEECs) is still unelucidated. The purpose of this experiment was to investigate the molecular mechanism of gEECs death caused by S. aureus in terms of autophagy and endoplasmic reticulum (ER) stress. We found that the accumulation of autophagosomes exacerbated S. aureus-induced gEECs apoptosis, and that ER stress was involved in the regulation of the autophagy. These findings may provide new insight into the therapeutic target of endometrial cell injury.Increasing evidence indicates that autophagy and endoplasmic reticulum (ER) stress are involved in the regulation of cell death; however, the role of autophagy and ER stress in Staphylococcus aureus-induced endometrial epithelial cell damage is still unelucidated. In the present study, our results showed that infection with S. aureus increased the cytotoxicity and the protein expression of Bax, caspase-3, and cleaved-PARP-1 in goat endometrial epithelial cells (gEECs). Moreover, after infection, the expression of LC3II and autophagosomes were markedly increased. The autophagosome inhibitor 3-methyladenine (3-MA) significantly decreased the cytotoxicity and the expression of caspase-3, and cleaved-PARP-1; however, the autophagosome–lysosome fusion inhibitor chloroquine (CQ) increased their expression. Additionally, the protein expression of GRP78, EIF2α, and ATF4 were also markedly increased after infection. The ER stress inhibitor 4-PBA decreased the cytotoxicity and the expression of LC3II and apoptosis-related proteins in S. aureus-infected gEECs. Collectively, our findings prove that the accumulation of autophagosomes exacerbated S. aureus-induced gEECs apoptosis, and that ER stress was involved in the regulation of the autophagy and apoptosis.
Highlights
Staphylococcus aureus is a recognized zoonotic disease pathogen, leading to a great threat to humans and animals
In order to investigate the effect of S. aureus on goat endometrial epithelial cells (gEECs) cytotoxicity, cells were infected with S. aureus (10 multiplicity of infection (MOI)) for 2 and 4 h
We performed a Western blot assay to determine the effect of S. aureus on gEECs apoptosis at the indicated time (4 h)
Summary
Staphylococcus aureus is a recognized zoonotic disease pathogen, leading to a great threat to humans and animals. The structural and functional integrity of the endometrium plays a key role in defending against pathogenic bacterial infections [1]. It is necessary to explore the toxicity mechanism of S. aureus on the uterus. Endometrial epithelial cells (EECs) are considered to be the first physical line of defense against pathogens that modulate innate immunity and inflammatory responses [2]. Revealing the mechanisms of damage to EECs is essential in order to control the occurrence and establishment of bacterial infections in the uterus. Studies have reported that S. aureus promotes nitric oxide release from endothelial and epithelial cells, the inward flow of extracellular Ca2+ , the production of pro-inflammatory cytokines, the activation of caspase-1 and NLRP3 inflammasome to promote pyroptosis, the cleavage of ligand proteins to disrupt epithelial cell barriers, 4.0/)
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