rhIL-32γ Facilitates Macrophage Phagocytosis of Streptococcus pneumoniae by Activating NF-κB-Soluble Epoxide Hydrolase Pathway.

Authors

Longying Liang, Tingting Li, Weiwei Zhang, Chengmin Deng, Longze Zhang, Kaifeng Wu, Shifei Yao

Published in

Journal of leukocyte biology. Jul 10, 2026. Epub Jul 10, 2026.

Abstract

Interleukin (IL)-32 is recognized as a potent proinflammatory mediator in various infectious contexts, however, its precise contribution to host defense against Streptococcus pneumoniae (S. pneumoniae) remains to be fully elucidated. This study demonstrates that S. pneumoniae challenge robustly upregulates IL-32 expression in human peripheral blood mononuclear cells and THP-1 cells. Functional assays reveal that exogenous recombinant human IL-32γ (rhIL-32γ) significantly potentiates the phagocytic activity of both murine (RAW 264.7) and human (THP-1-derived) macrophages against S. pneumoniae. Mechanistically, rhIL-32γ-induced phagocytosis is mediated by the upregulation and secretion of soluble epoxide hydrolase (sEH), a process contingent upon the activation of the nuclear factor kappa B (NF-κB) signaling pathway. Furthermore, pharmacological inhibition of either NF-κB or sEH effectively abrogates the pro-phagocytic effects of rhIL-32γ, confirming the functional requirement of the NF-κB-sEH axis in this response. Collectively, these results elucidate a novel IL-32γ-NF-κB-sEH regulatory cascade that facilitates macrophage-mediated bacterial clearance, thereby identifying a potential therapeutic target for the management of pneumococcal infections.

PMID:
42430657
Bibliographic data and abstract were imported from PubMed on 11 Jul 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.