PDCD4-mediated downregulation of burden in macrophages.

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.