The Autophagy Induced by Cryptosporidium Parvum Via Mtor Pathway in Hct-8 Cells
Autophagy is an important intracellular homeostatic mechanism beneficial for eliminating invading pathogens. Investigating the interaction between pathogens and cell autophagy can help us understand how these diseases occur and develop. In this study, HCT-8 cells were cultured with Cryptosporidium parvum (C. parvum), and C. parvum-induced autophagy was detected. The results showed that LC3II and Beclin-1 proteins were upregulated in HCT-8 cells co-cultured with C. parvum sporozoites, and the level of P62 protein was decreased. Immunofluorescence assays showed scattered LC3 fluorescent spots in HCT-8 cells infected with C. parvum. After transfection with EGFP-LC3, HCT-8 cells were cultured with C. parvum, and the results revealed that the fluorescent spots increased significantly in a time-dependent manner. In addition, when sporozoites resided in the parasitophorous vacuoles, autophagosome structure was observed in the cytoplasm by transmission electron microscopy. Data showed that the expression levels of phospho-PI3K, phospho-AKT, phospho-mTOR, and P62 were downregulated, while AMPK and ULK1 expression did not change significantly, indicating that C. parvum could induce autophagy in HCT-8 cells via the mTOR pathway. Moreover, the proliferation of C. parvum decreased on treating HCT-8 cells with the autophagy inducer rapamycin and increased on treating cells with the autophagy inhibitor 3-methyladenine at 12hr. In summary, autophagy can be induced by C. parvum in HCT-8 cells via the mTOR pathway, which prevents the early development of C. parvum. These data lay a foundation for further studies on the relationship between C. parvum and the host to control C. parvum infection.
| Medienart: |
E-Book |
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| Erscheinungsjahr: |
[2023] |
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| Erschienen: |
S.l.: SSRN ; 2023 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Yu, Qile [VerfasserIn] |
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| Links: |
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| Umfang: |
1 Online-Ressource (16 p) |
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| doi: |
10.2139/ssrn.4450401 |
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| Förderinstitution / Projekttitel: |
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| 520 | |a Autophagy is an important intracellular homeostatic mechanism beneficial for eliminating invading pathogens. Investigating the interaction between pathogens and cell autophagy can help us understand how these diseases occur and develop. In this study, HCT-8 cells were cultured with Cryptosporidium parvum (C. parvum), and C. parvum-induced autophagy was detected. The results showed that LC3II and Beclin-1 proteins were upregulated in HCT-8 cells co-cultured with C. parvum sporozoites, and the level of P62 protein was decreased. Immunofluorescence assays showed scattered LC3 fluorescent spots in HCT-8 cells infected with C. parvum. After transfection with EGFP-LC3, HCT-8 cells were cultured with C. parvum, and the results revealed that the fluorescent spots increased significantly in a time-dependent manner. In addition, when sporozoites resided in the parasitophorous vacuoles, autophagosome structure was observed in the cytoplasm by transmission electron microscopy. Data showed that the expression levels of phospho-PI3K, phospho-AKT, phospho-mTOR, and P62 were downregulated, while AMPK and ULK1 expression did not change significantly, indicating that C. parvum could induce autophagy in HCT-8 cells via the mTOR pathway. Moreover, the proliferation of C. parvum decreased on treating HCT-8 cells with the autophagy inducer rapamycin and increased on treating cells with the autophagy inhibitor 3-methyladenine at 12hr. In summary, autophagy can be induced by C. parvum in HCT-8 cells via the mTOR pathway, which prevents the early development of C. parvum. These data lay a foundation for further studies on the relationship between C. parvum and the host to control C. parvum infection | ||
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