C5a-regulated CCAAT/Enhancer-binding Proteins β and δ Are Essential in Fcγ Receptor-mediated Inflammatory Cytokine and Chemokine Production in Macrophages

Yan, Chunguang; Zhu, Mingzhao; Staiger, Jennifer; Johnson, Peter F.; Gao, Hongwei

doi:10.1074/jbc.m111.280834

Cited by 52 publications

(46 citation statements)

References 54 publications

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“…Matsuda et al (2010) demonstrated that transgenic mice overexpressing C/EBP␤ specifically in the pancreatic ␤ cell resulted in decreased ␤ cell mass and diabetes; while targeted disruption of C/EBP␤ in the pancreatic ␤ cell of obese or diabetic mice preserved ␤ cell mass and ameliorated hyperglycemia (25). These findings, combined with those of others (23,29), suggest that C/EBP␤ is central to the pathogenesis of several inflammatory disorders. While C/EBP␤ is a key regulator of metabolism, adipocyte differentiation, and macrophage activation, its pivotal role in the pathogenesis of dietary-induced inflammation remains relatively unexplored.…”

supporting

confidence: 50%

“…C/EBP␦ has been less characterized than C/EBP␤; however, unlike C/EBP␤, C/EBP␦ has been suggested to play a greater role in T regulatory cells and in dendritic cells found in the central nervous system (44). In contrast, macrophages deficient in either C/EBP␤ or C/EBP␦ failed to show a significant decrease in IL-6 and TNF␣ induction, suggesting compensatory roles of C/EBP␤ and C/EBP␦ in induction of pro-inflammatory cytokines (29,40,45). Given that mice lacking C/EBP␤ either globally or in bone marrow chimera studied here showed a striking reduction in inflammatory responses, suggests there is low redundancy in the system; however, this warrants further investigation.…”

Section: Discussionmentioning

confidence: 81%

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CCAAT/Enhancer-binding Protein β (C/EBPβ) Expression Regulates Dietary-induced Inflammation in Macrophages and Adipose Tissue in Mice

Rahman

Janssen

Choudhury

et al. 2012

Journal of Biological Chemistry

101

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Background: Role of CCAAT/enhancer-binding protein ␤ in obesity-induced inflammation remains unexplored. Results: Bone marrow-chimeric mice studies show that C/EBP␤ deletion regulates dietary-induced systemic inflammation and insulin resistance. Conclusion: C/EBP␤ expression in response to palmitate or high-fat diet controls transcriptional regulatory networks in macrophages and adipocytes critical for inflammation, lipid metabolism, and insulin resistance. Significance: Attenuating C/EBP␤ is an attractive target for ameliorating nutrition-induced inflammation.

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supporting

confidence: 50%

Section: Discussionmentioning

confidence: 81%

CCAAT/Enhancer-binding Protein β (C/EBPβ) Expression Regulates Dietary-induced Inflammation in Macrophages and Adipose Tissue in Mice

Rahman

Janssen

Choudhury

et al. 2012

Journal of Biological Chemistry

101

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“…In addition, our recent studies show that C/EBP transcription factors play a critical role in FcγR signaling in macrophages and IgG immune complex-induced lung injury (29, 30). To determine the potential mechanisms whereby p-RvD1 and AT-RvD1 suppress IgG immune complex-induced inflammation, we performed EMSA assay of nuclear proteins from control and IgG immune complex-injured lungs in the presence or absence of p-RvD1 or AT-RvD1 to evaluate NF-κB and C/EBP activation.…”

Section: Resultsmentioning

confidence: 99%

Protective Actions of Aspirin-Triggered (17R) Resolvin D1 and Its Analogue, 17R-Hydroxy-19-Para-Fluorophenoxy-Resolvin D1 Methyl Ester, in C5a-Dependent IgG Immune Complex–Induced Inflammation and Lung Injury

Tang

Liu

Yan

et al. 2014

The Journal of Immunology

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Increasing evidence suggests that the novel anti-inflammatory and pro-resolving mediators such as the resolvins play an important role during inflammation. However, the functions of these lipid mediators in immune complex (IC)-induced lung injury remain unknown. Here, we determined the role of aspirin-triggered resolvin D1 (AT-RvD1) and its metabolically stable analogue, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester (p-RvD1), in IgG IC-induced inflammatory responses in myeloid cells and injury in the lung. We show that lung vascular permeability in the AT-RvD1- or p-RvD1-treated mice were significantly reduced when compared with values in mice receiving control vesicle during the injury. Furthermore, i.v. administration of either AT-RvD1 or p-RvD1 caused significant decreases in the bronchoalveolar lavage fluids (BALF) contents of neutrophils, inflammatory cytokines, and chemokines. Of interest, AT-RvD1 or p-RvD1 significantly reduced BALF complement C5a level. By Electrophoretic Mobility Shift Assay, we demonstrate that IgG IC-induced activation of NF-κB and C/EBPβ transcription factors in the lung were significantly inhibited by AT-RvD1 and p-RvD1. Moreover, AT-RvD1 dramatically mitigates IgG IC-induced NF-κB and C/EBP activity in alveolar macrophages. Also, secretion of TNF-α, IL-6, KC, and MIP-1α from IgG IC-stimulated alveolar macrophages or neutrophils was significantly decreased by AT-RvD1. These results suggest a new approach to the blocking of IC-induced inflammation.

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“…Thus, C/EBP b may be a therapeutic target in brain injury and neurodegenerative disorders where excitotoxic neuronal cell death and inflammation are involved. Moreover, phosphorylation of ERK1/2 is involved in the induction of C/EBP b (14). TNF-a, a downstream target of C/EBP b, has been reported to be associated with neuropathological effects underlying several neurodegenerative disorders (15,16).…”

mentioning

confidence: 99%

Troxerutin Counteracts Domoic Acid–Induced Memory Deficits in Mice by Inhibiting CCAAT/Enhancer Binding Protein β–Mediated Inflammatory Response and Oxidative Stress

Lü

Zheng

et al. 2013

The Journal of Immunology

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The C/EBP β is a basic leucine zipper transcription factor that regulates a variety of biological processes, including metabolism, cell proliferation and differentiation, and immune response. Recent findings show that C/EBP β–induced inflammatory responses mediate kainic acid–triggered excitotoxic brain injury. In this article, we show that protein kinase C ζ enhances K-ras expression and subsequently activates the Raf/MEK/ERK1/2 pathway in the hippocampus of domoic acid (DA)–treated mice, which promotes C/EBP β expression and induces inflammatory responses. Elevated production of TNF-α impairs mitochondrial function and increases the levels of reactive oxygen species by IκB kinase β/NF-κB signaling. The aforementioned inflammation and oxidative stress lead to memory deficits in DA-treated mice. However, troxerutin inhibits cyclin-dependent kinase 1 expression, enhances type 1 protein phosphatase α dephosphorylation, and abolishes MEK/ERK1/2/C/EBP β activation, which subsequently reverses the memory impairment observed in the DA-treated mice. Thus, troxerutin is recommended as a potential candidate for the prevention and therapeutic treatment of cognitive deficits resulting from excitotoxic brain damage and other brain disorders.

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C5a-regulated CCAAT/Enhancer-binding Proteins β and δ Are Essential in Fcγ Receptor-mediated Inflammatory Cytokine and Chemokine Production in Macrophages

Cited by 52 publications

References 54 publications

CCAAT/Enhancer-binding Protein β (C/EBPβ) Expression Regulates Dietary-induced Inflammation in Macrophages and Adipose Tissue in Mice

CCAAT/Enhancer-binding Protein β (C/EBPβ) Expression Regulates Dietary-induced Inflammation in Macrophages and Adipose Tissue in Mice

Protective Actions of Aspirin-Triggered (17R) Resolvin D1 and Its Analogue, 17R-Hydroxy-19-Para-Fluorophenoxy-Resolvin D1 Methyl Ester, in C5a-Dependent IgG Immune Complex–Induced Inflammation and Lung Injury

Troxerutin Counteracts Domoic Acid–Induced Memory Deficits in Mice by Inhibiting CCAAT/Enhancer Binding Protein β–Mediated Inflammatory Response and Oxidative Stress

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