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Chlamydia trachomatis induces autophagy by p62 in HeLa cell

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World Journal of Microbiology and Biotechnology Aims and scope Submit manuscript

Abstract

Chlamydia trachomatis is the most common bacterial pathogen causing sexually transmitted diseases. C. trachomatis infection is closely related to the development of cervical cancer, studies have shown that C. trachomatis can induce host cell autophagy. The autophagy related gene p62 plays an important role in the process of autophagy. To further understand the role of autophagy-associated gene p62 in autophagy of HeLa cells induced by C. trachomatis, p62-silencing cell line, HeLa229-shp62, and control cell line, HeLa229-shNC, were constructed, and a C. trachomatis-infected cell model was established. The autophagosome and C. trachomatis inclusions were observed under electron microscope. The autophagy level of C. trachomatis-infected HeLa cells was detected by Western blot. The results suggested that knockdown of p62 affected neither C. trachomatis infection of HeLa cells nor the initiation of C. trachomatis-induced autophagy, but at 48 h post C. trachomatis infection, autophagy levels were significantly inhibited in p62 silencing host cells. The study demonstrated the important role of p62 in the autophagy induced by C. trachomatis in HeLa cells, which could provide data support and theoretical basis for exploring the pathogenesis and prevention of C. trachomatis.

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The data supporting the findings of this study are available within the article.

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Funding

This work was supported by National Natural Science Foundation of China (Grant Nos. 81371864, 81572040 and 81501791) and Natural Science Foundation of Hunan Province (2018JJ3819 and 2019JJ40392).

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Correspondence to Lei Zhang or Yong Wang.

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The authors declare no conflict of interest.

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The study was approved by the ethics committee of Xiangya School of medicine, Central South University.

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Wang, F., Zhang, H., Lu, X. et al. Chlamydia trachomatis induces autophagy by p62 in HeLa cell. World J Microbiol Biotechnol 37, 50 (2021). https://doi.org/10.1007/s11274-021-03014-5

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  • DOI: https://doi.org/10.1007/s11274-021-03014-5

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