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PDCD4-mediated downregulation of Listeria monocytogenes 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 (...

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Detalles Bibliográficos
Autores principales: Zhang, Xingju, Zhang, Jiale, Li, Fei, Luo, Yachen, Jiang, Shan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8056355/
https://www.ncbi.nlm.nih.gov/pubmed/33897282
http://dx.doi.org/10.5114/ceji.2021.105244
Descripción
Sumario: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.