Shao Lili, Zhang Tianyuan, Melero Jose, Huang Yumeng, Liu Yuanjun, Liu Quanzhong, He Cheng, Nelson David E, Zhong Guangming
Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Department of Dermatovenereology, Tianjin Medical University General Hospital, Tianjin, China.
Infect Immun. 2017 Dec 19;86(1). doi: 10.1128/IAI.00429-17. Print 2018 Jan.
The cryptic plasmid is essential for dissemination from the genital tract to the gastrointestinal (GI) tract. Following intravaginal inoculation, a strain deficient in plasmid-encoded pGP3 or pGP4 but not pGP5, pGP7, or pGP8 failed to spread to the mouse gastrointestinal tract, although mice infected with these strains developed productive genital tract infections. pGP3- or pGP4-deficient strains also failed to colonize the gastrointestinal tract when delivered intragastrically. pGP4 regulates pGP3, while pGP3 does not affect pGP4 expression, indicating that pGP3 is critical for colonization of the gastrointestinal tract. Mutants deficient in GlgA, a chromosome-encoded protein regulated by pGP4, also consistently colonized the mouse gastrointestinal tract. Interestingly, colonization of the gastrointestinal tract positively correlated with pathogenicity in the upper genital tract. pGP3-deficient strains did not induce hydrosalpinx or spread to the GI tract even when delivered to the oviduct by intrabursal inoculation. Thus, the current study not only has revealed that pGP3 is a novel chlamydial colonization factor in the gastrointestinal tract but also has laid a foundation for investigating the significance of gastrointestinal .
隐蔽质粒对于从生殖道传播至胃肠道至关重要。经阴道接种后,一株缺乏质粒编码的pGP3或pGP4但不缺乏pGP5、pGP7或pGP8的菌株无法传播至小鼠胃肠道,尽管感染这些菌株的小鼠发生了有繁殖力的生殖道感染。当经胃内接种时,缺乏pGP3或pGP4的菌株也无法在胃肠道定殖。pGP4调节pGP3,而pGP3不影响pGP4的表达,这表明pGP3对于胃肠道定殖至关重要。缺乏GlgA(一种受pGP4调节的染色体编码蛋白)的突变体也始终能够在小鼠胃肠道定殖。有趣的是,胃肠道定殖与上生殖道致病性呈正相关。缺乏pGP3的菌株即使通过囊内接种输送至输卵管也不会诱发输卵管积水或传播至胃肠道。因此,当前研究不仅揭示了pGP3是衣原体在胃肠道中的一种新型定殖因子,也为研究胃肠道的意义奠定了基础。