| Autor: |
Conrad, Turner Allen, Gong, Siqi, Yang, Zhangsheng, Matulich, Patrick, Keck, Jonathon, Beltrami, Noah, Chen, Chaoqun, Zhou, Zhou, Dai, Jin, Zhong, Guangming |
| Zdroj: |
Infection and Immunity; December 2015, Vol. 84 Issue: 2 p467-479, 13p |
| Abstrakt: |
ABSTRACTWe previously associated a missense mutation of the tc0668gene of serial in vitro-passaged Chlamydia muridarum, a murine model of human urogenital C. trachomatis, with severely attenuated disease development in the upper genital tract of female mice. Since these mutants also contained a TC0237 Q117E missense mutation that enhances their in vitroinfectivity, an effort was made here to isolate and characterize a tc0668single mutant to determine its individual contribution to urogenital pathogenicity. Detailed genetic analysis of C. muridarumpassages revealed a truncated variant with a G216* nonsense mutation of the 408-amino-acid TC0668 protein that does not produce a detectable product. Intracellular growth and infectivity of C. muridarum in vitroremain unaffected in the absence of TC0668. Intravaginal inoculation of the TC0668 null mutant into C3H/HeJ mice results in a typical course of lower genital tract infection but, unlike a pathogenic isogenic control, is unable to elicit significant chronic inflammation of the oviduct and fails to induce hydrosalpinx. Thus, TC0668 is demonstrated as an important chromosome-encoded urogenital pathogenicity factor of C. muridarumand the first with these characteristics to be discovered for a Chlamydiapathogen. |
| Databáze: |
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