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However, little is known about the regulation of human FHs 74 small intestinal epithelial cell viability in response to T. gondii infection. Here we show that T. gondii RH strain tachyzoite infection or ESP treatment of FHs 74 Int cells induced apoptosis, mitochondrial dysfunction and ER stress in host cells. Pretreatment with 4-PBA inhibited the expression or activation of key molecules involved in ER stress. In addition, both T. gondii and ESP challenge-induced mitochondrial dysfunction and cell death were dramatically suppressed in 4-PBA pretreated cells. Our study indicates that T. gondii infection induced ER stress in FHs 74 Int cells, which induced mitochondrial dysfunction followed by apoptosis. This may constitute a potential molecular mechanism responsible for the foodborne parasitic disease caused by T. gondii.<\/jats:p>","DOI":"10.3347\/kjp.2021.59.6.573","type":"journal-article","created":{"date-parts":[[2021,12,22]],"date-time":"2021-12-22T23:55:28Z","timestamp":1640217328000},"page":"573-583","update-policy":"https:\/\/doi.org\/10.3347\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Toxoplasma gondii Induces Apoptosis via Endoplasmic Reticulum Stress-Derived Mitochondrial Pathway in Human Small Intestinal Epithelial 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