Introduction
Macrophages are effector cells of the innate immune system and defend against invading pathogens. Previous reports have shown that infection with Listeria monocytogenes upregulates miR-21a expression in macrophages. Aim of the study: We aimed to verify whether programmed cell death 4 (PDCD4) is involved in the high bacterial burden observed in macrophages during late-stage L. monocytogenes infections.

Material and methods
We examined the expression of miR-21a and its known target PDCD4 in macrophages after L. monocytogenes infection. The macrophages’ uptake ability of L. monocytogenes was measured using FluoSpheres Carboxylate-modified microspheres. We depleted PDCD4 by transfecting macrophages with siPDCD4.

Results
In macrophages, PDCD4 protein was downregulated 5 h, but not 2 h, after L. monocytogenes infection. Our results validated the hypothesis that PDCD4-depleted macrophages present a higher L. monocytogenes burden. Moreover, we found that the activation of c-Jun and STAT3 accompanied PDCD4 downregulation.

Conclusions
Our results showed that PDCD4 mediated the suppression of L. monocytogenes infection in macrophages via c-Jun/STAT3 signalling activation.



中文翻译：

---

PDCD4介导的巨噬细胞单核细胞增生李斯特菌负荷下调

简介
巨噬细胞是先天免疫系统的效应细胞，可抵御入侵​​的病原体。先前的报道表明，单核细胞增生李斯特菌感染上调了巨噬细胞中 miR-21a 的表达。研究目的：我们旨在验证程序性细胞死亡 4 (PDCD4) 是否与晚期单核细胞增生李斯特菌感染期间巨噬细胞中观察到的高细菌负荷有关。

材料和方法
我们检测了单核细胞增生李斯特菌感染后巨噬细胞中 miR-21a 及其已知靶点 PDCD4 的表达。使用 FluoSpheres 羧酸盐修饰的微球测量巨噬细胞对单核细胞增生李斯特菌的摄取能力。我们通过用 siPDCD4 转染巨噬细胞来消耗 PDCD4。

结果
在巨噬细胞中，PDCD4 蛋白在单核细胞增生李斯特菌感染后 5 小时而不是 2 小时下调。我们的结果验证了 PDCD4 耗尽的巨噬细胞呈现出更高的单核细胞增生李斯特菌负担的假设。此外，我们发现 c-Jun 和 STAT3 的激活伴随着 PDCD4 的下调。

结论
我们的结果表明，PDCD4 通过 c-Jun/STAT3 信号激活介导抑制巨噬细胞中的单核细胞增生李斯特菌感染。