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首页> 外文期刊>Infection and immunity >Complement Factor C5 but Not C3 Contributes Significantly to Hydrosalpinx Development in Mice Infected with Chlamydia muridarum
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Complement Factor C5 but Not C3 Contributes Significantly to Hydrosalpinx Development in Mice Infected with Chlamydia muridarum

机译：补体因子C5但不是C3对感染衣原体衣原体的小鼠Hydrosalpinx发育有重要贡献。

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摘要

Hydrosalpinx is a pathological hallmark of tubal infertility associated with chlamydial infection. However, the mechanisms of hydrosalpinx remain unknown. Here, we report that complement factor 5 (C5) contributes significantly to chlamydial induction of hydrosalpinx. Mice lacking C5 (C5?/?) failed to develop any hydrosalpinx, while ～42% of the corresponding wild-type mice (C5+/+) did so following intravaginal infection with Chlamydia muridarum. Surprisingly, deficiency in C3 (C3?/?), an upstream component of the complement system, did not affect mouse susceptibility to chlamydial induction of hydrosalpinx. Interestingly, C5 activation was induced by chlamydial infection in oviducts of C3?/? mice, explaining why the C3?/? mice remained susceptible to chlamydial induction of hydrosalpinx. Similar levels of live chlamydial organisms were recovered from oviduct tissues of both C5?/? and C5+/+ mice, suggesting that C5 deficiency did not affect C. muridarum ascending infection. Furthermore, C5?/? mice were still more resistant to hydrosalpinx induction than C5+/+ mice, even when live C. muridarum organisms were directly delivered into the upper genital tract, both confirming the role of C5 in promoting hydrosalpinx and indicating that the C5-facilitated hydrosalpinx was not due to enhancement of ascending infection. The C5?/? mice displayed significantly reduced lumenal inflammatory infiltration and cytokine production in oviduct tissue, suggesting that C5 may contribute to chlamydial induction of hydrosalpinx by enhancing inflammatory responses.
机译：输卵管积水是与衣原体感染相关的输卵管不育的病理标志。然而，输卵管积水的机制仍然未知。在这里，我们报告补体因子5（C5）大大有助于衣原体的衣原体诱导。缺乏C5的小鼠（C5 ？/？）未能发育出任何输卵管积水，而约42％的相应野生型小鼠（C5 + / + ）则在阴道内这样做感染衣原体。令人惊讶地，补体系统上游成分C3（C3 ？/？）的缺乏并未影响小鼠对输卵管积水的衣原体诱导的敏感性。有趣的是，衣原体感染在C3 ？/？小鼠的输卵管中诱导了C5的激活，这解释了为什么C3 ？/？小鼠仍然易感衣原体诱导输卵管积水。从C5 ？/？和C5 + / + 小鼠的输卵管组织中回收到相似水平的衣原体生物体，这表明C5缺乏并不影响墨角衣原体上升感染。 。此外，即使将活的衣原体衣原体微生物直接递送到上生殖道中，C5 ？/？小鼠比C5 + / + 小鼠对水salpinx诱导的抵抗力仍然更高。 ，既证实了C5在促进输卵管积水中的作用，也表明C5促进的输卵管积水不是由于上升感染的增强。 C5 ？/？小鼠在输卵管组织中显示出明显降低的管腔炎性浸润和细胞因子产生，表明C5可能通过增强炎症反应来促进衣原体诱导衣原体的形成。

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