Infectivity of urogenital Chlamydia trachomatis plasmid-deficient, CT135-null, and double-deficient strains in female mice.
Infectivity of urogenital Chlamydia trachomatis plasmid-deficient, CT135-null, and double-deficient strains in female mice.
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DOI：
10.1111/2049-632x.12121
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发表时间：
2014-06
影响因子：
3.3
通讯作者：
Caldwell HD
中科院分区：
文献类型：
--
作者：
Sturdevant GL;Zhou B;Carlson JH;Whitmire WM;Song L;Caldwell HD
沙眼衣原体是人类细菌性传播感染的最常见原因，也是世界上可预防的传染性失明的主要原因。在非人灵长类动物和小鼠感染模型中，衣原体7.5 kb质粒和染色体基因CT135已被证明是重要的毒力因子。沙眼衣原体质粒缺失泌尿生殖道分离株和预测的CT135零突变株已经在雌性小鼠生殖道模型中独立评估，两者都显示出降低传染性和毒力。然而，这些衰减表型尚未在小鼠模型中进行集体评估。在这里，我们在小鼠模型中测试了沙眼衣原体血清型D菌株的传染性，这些菌株是质粒缺陷、CT135破坏或具有这些减毒基因型的组合。我们发现，质粒的存在导致感染具有更高的感染负担，而CT135促进更持久或慢性感染。不出所料，这些遗传缺陷的结合导致菌株具有增强的感染衰减特性。
Chlamydia trachomatis is the most common cause of human bacterial sexually transmitted infections and is the world’s leading cause of infectious preventable blindness. The chlamydial 7.5 kb plasmid and chromosomal gene CT135 have been shown to be important virulence factors in both nonhuman primate and mouse infection models. C. trachomatis plasmid-deficient urogenital isolates and a predicted CT135 null mutant have been evaluated independently in the female mouse genital tract model and both have been shown to reduce infectivity and virulence. However, these attenuating phenotypes have not been evaluated collectively in the murine model. Here, we test the infectivity of C. trachomatis serovar D strains in the mouse model that are plasmid-deficient, CT135 disrupted, or possess a combination of these attenuating genotypes. We find that the presence of the plasmid results in infections with higher infectious burdens whereas CT135 facilitates a more protracted or chronic infection. Not unexpectedly, a combination of these genetic deficiencies resulted in a strain with enhanced infection attenuation characteristics.