Chlamydial Plasmid-Dependent Pathogenicity
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- 作者：Guangming Zhong1 ; Zhongg@UTHSCSA.edu
- 刊名：Trends in Microbiology
- 出版年：2017
- 出版时间：February 2017
- 年：2017
- 卷：25
- 期：2
- 页码：141-152
- 全文大小：1553 K
- 卷排序：25
文摘
Most Chlamydia species carry a 7.5 kb plasmid encoding eight open reading frames conventionally called plasmid glycoproteins 1–8 or pGP1–8. Although the plasmid is not critical for chlamydial growth in vitro, its role in chlamydial pathogenesis is clearly demonstrated in the genital tracts of mice infected with Chlamydia muridarum, a model for investigating the human pathogen Chlamydia trachomatis. Plasmid-free C. trachomatis is also attenuated in both the mouse genital tract and nonhuman primate ocular tissue. Deficiency in pGP3 alone, which is regulated by pGP4, largely reproduced the in vivo but not in vitro phenotypes of the plasmid-free organisms, suggesting that pGP3 is a key in vivo virulence factor. The positive and negative regulations of some chromosomal genes by pGP4 and pGP5, respectively, may allow the plasmid to promote chlamydial adaptation to varied animal tissue environments. The focus of this review is to summarize the progress on the pathogenic functions of the plasmid-encoded open reading frames, which may motivate further investigation of the molecular mechanisms of chlamydial pathogenicity and development of medical utility of the chlamydial plasmid system.