The inflammatory response to Chlamydia infection is likely to be multifactorial and involve a variety of ligand-dependent and -independent recognition pathways. We previously reported the presence of NOD1/NOD2-dependent endoplasmic reticulum (ER) stress-induced inflammation during Chlamydia muridarum infection in vitro, but the relevance of this finding to an in vivo context is unclear. Here, we examined the ER stress response to in vivo Chlamydia infection. The induction of interleukin 6 (IL-6) production after systemic Chlamydia infection correlated with expression of ER stress response genes. Furthermore, when tauroursodeoxycholate (TUDCA) was used to inhibit the ER stress response, an increased bacterial burden was detected, suggesting that ER stress-driven inflammation can contribute to systemic bacterial clearance. Mice lacking both NOD1 and NOD2 or RIP2 exhibited slightly higher systemic bacterial burdens after infection with Chlamydia. Overall, these data suggest a model where RIP2 and NOD1/NOD2 proteins link ER stress responses with the induction of Chlamydia-specific inflammatory responses.

中文翻译：

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NOD1/NOD2 和 RIP2 在衣原体感染期间调节内质网应激诱导的炎症。

对衣原体感染的炎症反应可能是多因素的，涉及多种配体依赖性和非依赖性识别途径。我们之前报道了在体外鼠衣原体感染期间存在 NOD1/NOD2 依赖性内质网 (ER) 应激诱导的炎症，但这一发现与体内环境的相关性尚不清楚。在这里，我们检查了对体内衣原体感染的 ER 应激反应。全身性衣原体感染后白细胞介素 6 (IL-6) 产生的诱导感染与 ER 应激反应基因的表达相关。此外，当使用牛磺熊去氧胆酸盐 (TUDCA) 抑制 ER 应激反应时，检测到细菌负荷增加，这表明 ER 应激驱动的炎症有助于全身细菌清除。缺乏 NOD1 和 NOD2 或 RIP2 的小鼠在感染衣原体后表现出稍高的全身细菌负荷。总体而言，这些数据表明了一个模型，其中 RIP2 和 NOD1/NOD2 蛋白将 ER 应激反应与衣原体特异性炎症反应的诱导联系起来。