Research question

It is not clear whether innate immunity along with autophagy is altered in endometrial cells of patients with endometriosis.

Design

This study evaluated the effects of lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid (poly I:C) stimulation on autophagy induction, pro-IL-1β expression, and secretion of interleukin-1β (IL-1β) and tumour necrosis factor-α (TNFα) in endometrial epithelial and/or stromal cells of patients with endometriosis (EE-endo, ES-endo, respectively), those of patients with hydrosalpinx (EE-hydro, ES-hydro, respectively) and those of healthy fertile women (EE-healthy, ES-healthy, respectively), with and without inhibition of autophagy by autophagy-related (ATG)13 gene small interfering RNA (siRNA).

Results

Stimulation with either LPS or poly I:C triggered autophagy in EE/ES-healthy, whereas no significant induction was observed in either EE/ES-endo or EE/ES-hydro. In EE- and/or ES-healthy, IL-1β and/or TNFα secretion after stimulation with LPS or poly I:C was significantly higher in cells with ATG13 knockdown compared with those with siRNA control (P < 0.03), whereas no significant difference was observed in either EE/ES-endo or EE/ES-hydro. In the secretory phase ES-endo without autophagy inhibition, IL-1β and TNFα secretion were significantly higher compared with those of ES-healthy after stimulation with either LPS or poly I:C for 4 h (P < 0.001) and for 24 h (P < 0.01).

Conclusion

Pathogen-induced autophagy was impaired in EE/ES-endo. Increased IL-1β and TNFα release in response to pathogenic triggers in the secretory phase ES-endo may result in the development of an inflammatory uterine microenvironment detrimental to successful embryo implantation.

中文翻译：

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子宫内膜异位症患者分泌期子宫内膜基质细胞中病原体诱导的自噬受损并增加IL-1β和TNFα释放以响应致病触发

研究问题

目前尚不清楚子宫内膜异位症患者的子宫内膜细胞中的先天免疫和自噬是否发生改变。

设计

本研究评估了脂多糖 (LPS) 或聚肌苷酸: 聚胞苷酸 (poly I:C) 刺激对自噬诱导、pro-IL-1β 表达以及白细胞介素-1β (IL-1β) 和肿瘤坏死因子-α 分泌的影响子宫内膜异位症患者（分别为 EE-endo、ES-endo）、输卵管积水患者（分别为 EE-hydro、ES-hydro）和健康可育女性的子宫内膜上皮和/或基质细胞中的（TNFα）（分别为 EE-healthy、ES-healthy)，有和没有自噬相关 (ATG)13 基因小干扰 RNA (siRNA) 抑制自噬。

结果

用 LPS 或 poly I:C 刺激在 EE/ES-healthy 中触发自噬，而在 EE/ES-endo 或 EE/ES-hydro 中未观察到显着诱导。在 EE 和/或 ES 健康组中，与 siRNA 对照相比，LPS 或 poly I:C 刺激后的 IL-1β 和/或 TNFα 分泌在 ATG13 敲低的细胞中显着更高（P  < 0.03），而没有显着性在 EE/ES-endo 或 EE/ES-hydro 中观察到差异。在没有自噬抑制的分泌期 ES-endo 中，在用 LPS 或 poly I:C 刺激 4 小时（P  < 0.001）和 24 小时后，IL-1β 和 TNFα 的分泌显着高于 ES-healthy。P  < 0.01)。

结论

病原体诱导的自噬在 EE/ES-endo 中受损。在分泌期 ES-endo 中，IL-1β 和 TNFα 释放增加，可能会导致炎症性子宫微环境的发展，这对成功胚胎植入不利。