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.