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