Bibliographic Details
| Title: |
Pseudomonas aeruginosa -Derived DnaJ Induces the Expression of IL−1β by Engaging the Interplay of p38 and ERK Signaling Pathways in Macrophages. |
| Authors: |
Kim, Dae-Kyum1,2 (AUTHOR) eorua1110@korea.ac.kr, Huh, Jin-Won1 (AUTHOR) huh1056@korea.ac.kr, Yu, Hyeonseung1 (AUTHOR) cockychild74@naver.com, Lee, Yeji1 (AUTHOR) yejee90@korea.ac.kr, Jin, Yongxin3 (AUTHOR) yxjin@nankai.edu.cn, Ha, Un-Hwan1,2 (AUTHOR) haunhwan@korea.ac.kr |
| Source: |
International Journal of Molecular Sciences. Nov2023, Vol. 24 Issue 21, p15957. 13p. |
| Subject Terms: |
*HEAT shock proteins, *CELLULAR signal transduction, *SEPTIC shock, *MACROPHAGES, *QUORUM sensing, *NLRP3 protein, *MICROCYSTIS aeruginosa |
| Abstract: |
As members of pathogen-associated molecular patterns, bacterial heat shock proteins (HSPs) are widely recognized for their role in initiating innate immune responses. This study aimed to examine the impact of DnaJ, a homolog of HSP40 derived from Pseudomonas aeruginosa (P. aeruginosa), on the regulation of IL−1β expression in macrophages. We demonstrated that DnaJ modulates macrophages to secrete IL−1β by activating NF-κB and MAPK signaling pathways. Specifically, ERK was identified as a positive mediator for IL−1β expression, while p38 acted as a negative mediator. These results suggest that the reciprocal actions of these two crucial MAPKs play a vital role in controlling IL−1β expression. Additionally, the reciprocal actions of MAPKs were found to regulate the activation of inflammasome-related molecules, including vimentin, NLRP3, caspase-1, and GSDMD. Furthermore, our investigation explored the involvement of CD91/CD40 in ERK signaling-mediated IL−1β production from DnaJ-treated macrophages. These findings emphasize the importance of understanding the signaling mechanisms underlying IL−1β induction and suggest the potential utility of DnaJ as an adjuvant for stimulating inflammasome activation. [ABSTRACT FROM AUTHOR] |
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