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Published on: November 27, 2014
Recombinant human interleukin-32γ facilitates macrophage phagocytosis of Streptococcus pneumoniae by activating
Longying Liang1, Tingting Li1, Weiwei Zhang2
1Department of Laboratory Medicine, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), No. 98 Fenghuang Road, HuiChuan District, Zunyi, Guizhou Province 563000, China.
Abstract:
Interleukin-32 is recognized as a potent proinflammatory mediator in various infectious contexts; however, its precise contribution to host defense against Streptococcus pneumoniae (S.pn) remains to be fully elucidated. This study demonstrates that S.pn challenge robustly upregulates interleukin-32 expression in human peripheral blood mononuclear cells and THP-1 cells. Functional assays reveal that exogenous recombinant human interleukin-32γ significantly potentiates the phagocytic activity of both murine (RAW 264.7) and human (THP-1-derived) macrophages against S.pn. Mechanistically, recombinant human interleukin-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 κB (NF-κB) signaling pathway. Furthermore, pharmacological inhibition of either NF-κB or sEH effectively abrogates the prophagocytic effects of recombinant human interleukin-32γ, confirming the functional requirement of the NF-κB-sEH axis in this response. Collectively, these results elucidate a novel interleukin-32γ-NF-κB-sEH regulatory cascade that facilitates macrophage-mediated bacterial clearance, thereby identifying a potential therapeutic target for the management of pneumococcal infections.
Insights
Interleukin-32 (IL-32) enhances macrophage ability to clear Streptococcus pneumoniae. This involves the NF-κB pathway and soluble epoxide hydrolase (sEH), offering a new target for pneumococcal infection treatment.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Interleukin-32 (IL-32) is a proinflammatory cytokine with roles in various infections.
- Its specific function in host defense against Streptococcus pneumoniae (S. pneumoniae) requires further investigation.
Purpose of the Study:
- To investigate the role of IL-32 in host defense against S. pneumoniae.
- To elucidate the molecular mechanisms underlying IL-32's effect on macrophage function during pneumococcal infection.
Main Methods:
- S. pneumoniae challenge was used to induce IL-32 expression in human peripheral blood mononuclear cells and THP-1 cells.
- Functional assays assessed the impact of recombinant human IL-32γ (rhIL-32γ) on macrophage phagocytic activity.
- The study utilized NF-κB and sEH pathway inhibitors to explore the mechanistic basis of rhIL-32γ's effects.
Main Results:
- S. pneumoniae infection significantly increased IL-32 expression.
- rhIL-32γ enhanced the phagocytosis of S. pneumoniae by both murine and human macrophages.
- This enhancement was mediated by the upregulation and secretion of soluble epoxide hydrolase (sEH) via NF-κB pathway activation.
- Inhibition of NF-κB or sEH abolished the pro-phagocytic effects of rhIL-32γ.
Conclusions:
- A novel IL-32γ-NF-κB-sEH regulatory cascade enhances macrophage-mediated clearance of S. pneumoniae.
- This pathway represents a potential therapeutic target for managing pneumococcal infections.
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