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IL-1β-driven neutrophilia preserves antibacterial defense in the absence of the kinase IKKβ
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IL-1β-driven neutrophilia preserves antibacterial defense in the absence of the kinase IKKβ
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Journal Article
IL-1β-driven neutrophilia preserves antibacterial defense in the absence of the kinase IKKβ
2011
Overview
Pathways dependent on the transcription factor NF-κB provide innate immunity against microbes. Karin and colleagues show that mice lacking the kinase IKKβ have IL-1-dependent neutrophilia. Loss of IL-1 signaling restores blood cellularity but severely compromises antimicrobial defense.
Transcription factor NF-κB and its activating kinase IKKβ are associated with inflammation and are believed to be critical for innate immunity. Despite the likelihood of immune suppression, pharmacological blockade of IKKβ–NF-κB has been considered as a therapeutic strategy. However, we found neutrophilia in mice with inducible deletion of IKKβ (
Ikkβ
Δ
mice). These mice had hyperproliferative granulocyte-macrophage progenitors and pregranulocytes and a prolonged lifespan of mature neutrophils that correlated with the induction of genes encoding prosurvival molecules. Deletion of interleukin 1 receptor 1 (IL-1R1) in
Ikkβ
Δ
mice normalized blood cellularity and prevented neutrophil-driven inflammation. However,
Ikkβ
Δ
Il1r1
−/−
mice, unlike
Ikkβ
Δ
mice, were highly susceptible to bacterial infection, which indicated that signaling via IKKβ–NF-κB or IL-1R1 can maintain antimicrobial defenses in each other's absence, whereas inactivation of both pathways severely compromises innate immunity.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animals
/ Bacterial Infections - immunology
/ Biomedical and Life Sciences
/ Cell Growth Processes - genetics
/ Granulocyte-Macrophage Progenitor Cells - immunology
/ Granulocyte-Macrophage Progenitor Cells - metabolism
/ Granulocyte-Macrophage Progenitor Cells - pathology
/ I-kappa B Kinase - immunology
/ I-kappa B Kinase - metabolism
/ Interleukin-1beta - immunology
/ Interleukin-1beta - metabolism
/ Mice
