Mol Immunol. 2017 Jan 30;83:137-146. doi: 10.1016/j.molimm.2017.01.021. [Epub ahead of print]

DnaJ (hsp40) of Streptococcus pneumoniae is involved in bacterial virulence and elicits a strong natural immune reaction via PI3K/JNK.

Cui J1, Ma C2, Ye G3, Shi Y4, Xu W2, Zhong L2, Wang J2, Yin Y2, Zhang X5, Wang H6.

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Abstract

As a heat shock protein, DnaJ plays an important role in the pathogenesis of pneumococcal infection. However, how the virulence factor-DnaJ elicits host natural immunity still remains unclear. In this study, we investigated the effects of dnaJ deficiency in Streptococcus pneumoniae (S. pneumoniae) on bacterial virulence, and further explored the related molecular mechanisms in vivo and in vitro. By generating dnaJ deficient mutant (ΔdnaJ), the virulence and colonization were detected in murine pneumonia and sepsis models in vivo. Compared with wild-type parent strain, the abilities of rapid colonization and induction of inflammatory responses of ΔdnaJ in mouse lungs were significantly impaired. Simultaneously, recombinant DnaJ purified from E. coli expression system (rDnaJ) induced macrophage strain RAW264.7 to secrete IL-6 by activation of PI3K and JNK signal pathways, which were confirmed by the specific signaling inhibitors. In conclusion, DnaJ, a novel virulence protein, was essential for the virulence and colonization of S. pneumoniae and induced pro-inflammatory cytokine production in macrophages through PI3K/JNK.

Copyright © 2017 Elsevier Ltd. All rights reserved.

KEYWORDS:

DnaJ; IL-6; JNK; PI3K; Streptococcus pneumoniae

PMID: 28152394 DOI: 10.1016/j.molimm.2017.01.021

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