Intrauterine Infection with Plasmid-Free Chlamydia muridarum Reveals a Critical Role of the Plasmid in Chlamydial Ascension and Establishes a Model for Evaluating Plasmid-Independent Pathogenicity
Intrauterine Infection with Plasmid-Free Chlamydia muridarum Reveals a Critical Role of the Plasmid in Chlamydial Ascension and Establishes a Model for Evaluating Plasmid-Independent Pathogenicity
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DOI：
10.1128/iai.00353-15
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发表时间：
2015-06-01
影响因子：
3.1
通讯作者：
Zhong, Guangming
中科院分区：
文献类型：
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作者：
Chen, Jianlin;Yang, Zhangsheng;Zhong, Guangming
携带质粒而非携带质粒的muridarum衣原体阴道内感染可诱导小鼠上生殖道输卵管积水，表明质粒在衣原体致病性中起关键作用。为了评估质粒对衣原体提升和输卵管炎症激活的贡献，我们通过宫内接种将无质粒的muridarum直接送入子宫内膜。我们发现，当体外接种1 × 10(7)个不含质粒的muridarum包涵形成单位（IFU）时，6株小鼠中有3株（CBA/J、C3H/HeJ和C57BL/6J）出现了明显的滑膜积水。即使当接种量减少到1 × 10(4) IFU时，CBA/J小鼠仍然产生强健的输卵管积水。CBA/J小鼠输卵管积水的发生与宫内接种后生物体上升到输卵管的增加有关。CBA/J小鼠经阴道内感染相同的无质粒muridarum菌株后，上升感染减少，未发生输卵管积水。这些观察结果证明了质粒在衣原体上升感染中的关键作用。与阴道内接种相比，在CBA/J小鼠宫内接种无质粒的muridarum不仅导致了更多的输卵管感染，而且在输卵管内刺激了更多的炎症浸润和细胞因子的产生，这表明输卵管炎症可能是由质粒非依赖性因素引起的。由此可见，子宫内感染无质粒muridarum诱导CBA/J小鼠输卵管积水是研究不依赖质粒致病机制的合适模型。
Intravaginal infection with plasmid-competent but not plasmid-free Chlamydia muridarum induces hydrosalpinx in mouse upper genital tract, indicating a critical role of the plasmid in chlamydial pathogenicity. To evaluate the contribution of the plasmid to chlamydial ascension and activation of tubal inflammation, we delivered plasmid-free C. muridarum directly into the endometrium by intrauterine inoculation. We found that three of the six mouse strains tested, including CBA/J, C3H/HeJ, and C57BL/6J, developed significant hydrosalpinges when 1 x 10(7) inclusion-forming units (IFU) of plasmid-free C. muridarum were intrauterinally inoculated. Even when the inoculum was reduced to 1 x 10(4) IFU, the CBA/J mice still developed robust hydrosalpinx. The hydrosalpinx development in CBA/J mice correlated with increased organism ascension to the oviduct following the intrauterine inoculation. The CBA/J mice intravaginally infected with the same plasmid-free C. muridarum strain displayed reduced ascending infection and failed to develop hydrosalpinx. These observations have demonstrated a critical role of the plasmid in chlamydial ascending infection. The intrauterine inoculation of the CBA/J mice with plasmid-free C. muridarum not only resulted in more infection in the oviduct but also stimulated more inflammatory infiltration and cytokine production in the oviduct than the intravaginal inoculation, suggesting that the oviduct inflammation can be induced by plasmid-independent factors, which makes the hydrosalpinx induction in CBA/J mice by intrauterine infection with plasmid-free C. muridarum a suitable model for investigating plasmid-independent pathogenic mechanisms.