scholarly journals Prototypical anti-inflammatory cytokine IL-10 prevents loss of IGF-I-induced myogenin protein expression caused by IL-1β

2008 ◽  
Vol 294 (4) ◽  
pp. E709-E718 ◽  
Author(s):  
Klemen Strle ◽  
Robert H. McCusker ◽  
Rodney W. Johnson ◽  
Samantha M. Zunich ◽  
Robert Dantzer ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Muscle Wasting ◽  
Inflammatory Responses ◽  
Mapk Signaling ◽  
Protective Role ◽  
Igf I ◽  
Anti Inflammatory ◽  
Kinase Pathway ◽  
Anti Inflammatory Cytokine

Prolonged and excessive inflammation is implicated in resistance to the biological actions of IGF-I and contributes to the pathophysiology of neurodegenerative, metabolic, and muscle-wasting disorders. IL-10 is a critical anti-inflammatory cytokine that restrains inflammatory responses in macrophages and T cells by inhibiting cytokine and chemokine synthesis and reducing expression of their receptors. Here we demonstrate that IL-10 plays a protective role in nonhematopoietic cells by suppressing the ability of exogenous IL-1β to inhibit IGF-I-induced myogenin and myosin heavy chain expression in myoblasts. This action of IL-10 is not caused by impairment of IL-1β-induced synthesis of IL-6 or the ability of IL-1β to activate two members of the MAPK family, ERK1/2 and p38. Instead, this newly defined protective role of IL-10 occurs by specific reversal of IL-1β activation of the JNK kinase pathway. IL-10 blocks IL-1β-induced phosphorylation of JNK, but not ERK1/2 or p38, indicating that only the JNK component of the IL-1β-induced MAPK signaling pathway is targeted by IL-10. This conclusion is supported by the finding that a specific JNK inhibitor acts similarly to IL-10 to restore IGF-I-induced myogenin expression, which is suppressed by IL-1β. Collectively, these data demonstrate that IL-10 acts in a novel, nonclassical, protective manner in nonhematopoietic cells to inhibit the IL-1β receptor-induced JNK kinase pathway, resulting in prevention of IGF-I resistance.

scholarly journals Protective Role of C3aR (C3a Anaphylatoxin Receptor) Against Atherosclerosis in Atherosclerosis-Prone Mice

2020 ◽  
Vol 40 (9) ◽  
pp. 2070-2083
Author(s):  
Lin-Lin Wei ◽  
Ning Ma ◽  
Kun-Yi Wu ◽  
Jia-Xing Wang ◽  
Teng-Yue Diao ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Macrophage Polarization ◽  
Protective Role ◽  
Plaque Burden ◽  
Aortic Tissue ◽  
M2 Macrophage ◽  
Proinflammatory Mediators ◽  
Anti Inflammatory

Objective: Emerging evidence suggests that C3aR (C3a anaphylatoxin receptor) signaling has protective roles in various inflammatory-related diseases. However, its role in atherosclerosis has been unknown. The purpose of the study was to investigate the possible protective role of C3aR in aortic atherosclerosis and explore molecular and cellular mechanisms involved in the protection. Approach and Results: C3ar −/− /Apoe −/− mice were generated by cross-breeding of atherosclerosis-prone Apoe −/− mice and C3ar −/− mice. C3ar −/− /Apoe −/− mice and Apoe −/− mice (as a control) underwent high-fat diet for 16 weeks were assessed for (1) atherosclerotic plaque burden, (2) aortic tissue inflammation, (3) recruitment of CD11b + leukocytes into atherosclerotic lesions, and (4) systemic inflammatory responses. Compared with Apoe −/− mice, C3ar −/− /Apoe −/− mice developed more severe atherosclerosis. In addition, C3ar −/− /Apoe −/− mice have increased local production of proinflammatory mediators (eg, CCL2 [chemokine (C-C motif) ligand 2], TNF [tumor necrosis factor]-α) and infiltration of monocyte/macrophage in aortic tissue, and their lesional macrophages displayed an M1-like phenotype. Local pathological changes were associated with enhanced systemic inflammatory responses (ie, elevated plasma levels of CCL2 and TNF-α, increased circulating inflammatory cells). In vitro analyses using peritoneal macrophages showed that C3a stimulation resulted in upregulation of M2-associated signaling and molecules, but suppression of M1-associated signaling and molecules, supporting the roles of C3a/C3aR axis in mediating anti-inflammatory response and promoting M2 macrophage polarization. Conclusions: Our findings demonstrate a protective role for C3aR in the development of atherosclerosis and suggest that C3aR confers the protection through C3a/C3aR axis–mediated negative regulation of proinflammatory responses and modulation of macrophage toward the anti-inflammatory phenotype.

IL-37 (IL-1F7) the Newest Anti-Inflammatory Cytokine Which Suppresses Immune Responses and Inflammation

2012 ◽  
Vol 25 (1) ◽  
pp. 31-38 ◽  
Author(s):  
S. Tetè ◽  
D. Tripodi ◽  
M. Rosati ◽  
F. Conti ◽  
G. Maccauro ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Immune Responses ◽  
Proinflammatory Cytokines ◽  
Mechanism Of Action ◽  
Inflammatory Cytokine ◽  
Inflammatory Responses ◽  
Detailed Mechanism ◽  
Anti Inflammatory ◽  
And Function ◽  
Anti Inflammatory Cytokine

Cytokines such as interleukins, chemokines and interferons are immunomodulating and inflammatory agents, characterized by considerable redundancy, in that many cytokines appear to share similar functions. Virtually all nucleated cells, but especially epithelial cells and macrophages, are potent producers of cytokines. The objective of this study is to review the detailed mechanism of action and the biological profiles of IL-37, the newest anti-inflammatory cytokine. This review focuses on IL-37, a key cytokine in regulating inflammatory responses, mainly by inhibiting the expression, production and function of proinflammatory cytokines: IL-1 family pro-inflammatory effects are markedly suppressed by IL-37.

scholarly journals Functionally distinct subsets of human FOXP3+ Treg cells that phenotypically mirror effector Th cells

Blood ◽  
2012 ◽  
Vol 119 (19) ◽  
pp. 4430-4440 ◽  
Author(s):  
Thomas Duhen ◽  
Rebekka Duhen ◽  
Antonio Lanzavecchia ◽  
Federica Sallusto ◽  
Daniel J. Campbell
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Responses ◽  
Treg Cells ◽  
Receptor Expression ◽  
Inflammatory Cytokine Production ◽  
Th Cell ◽  
Different Types ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

Abstract FOXP3+ regulatory T (Treg) cells are a broadly acting and potent anti-inflammatory population of CD4+ T cells essential for maintaining immune homeostasis and preventing debilitating autoimmunity. Based on chemokine receptor expression, we identified distinct populations of Treg cells in human blood expected to colocalize with different Th cell subsets. Although each population was functionally suppressive, they displayed unique patterns of pro- and anti-inflammatory cytokine production, differentially expressed lineage-specifying transcription factors, and responded differently to antigens associated with Th1 and Th17 responses. These results highlight a previously unappreciated degree of phenotypic and functional diversity in human Treg cells that allows subsets with unique specificities and immunomodulatory functions to be targeted to defined immune environments during different types of inflammatory responses.

scholarly journals Novel activity of an anti-inflammatory cytokine: IL-10 prevents TNFα-induced resistance to IGF-I in myoblasts

2007 ◽  
Vol 188 (1-2) ◽  
pp. 48-55 ◽  
Author(s):  
Klemen Strle ◽  
Robert H. MCusker ◽  
Lynn Tran ◽  
Alexandra King ◽  
Rodney W. Johnson ◽  
...  
Keyword(s):  
Induced Resistance ◽  
Inflammatory Cytokine ◽  
Igf I ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

Genetic susceptibility to Graves’ ophthalmopathy: The role of polymorphisms in anti-inflammatory cytokine genes

2010 ◽  
Vol 31 (4) ◽  
pp. 215-220 ◽  
Author(s):  
Omid Khalilzadeh ◽  
Mehdi Anvari ◽  
Alireza Esteghamati ◽  
Fatemeh Momen-Heravi ◽  
Armin Rashidi ◽  
...  
Keyword(s):  
Genetic Susceptibility ◽  
Inflammatory Cytokine ◽  
Cytokine Genes ◽  
Graves Ophthalmopathy ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

scholarly journals The Strand Specific Regulation of miR-155-3p in Response to Lipopolysaccharide and Interleukin-10 Stimulation Requires FUBP1 Protein

2021 ◽  
Author(s):  
Jeff S. J. Yoon ◽  
Abdulwadood Baksh ◽  
Thomas C. Chamberlain ◽  
Alice L-F. Mui
Keyword(s):  
Inflammatory Cytokine ◽  
Inflammatory Responses ◽  
Interleukin 10 ◽  
Activated Macrophages ◽  
Anti Inflammatory ◽  
Specific Regulation ◽  
Anti Inflammatory Cytokine

MicroRNA-155 (miR-155) expression promotes inflammatory responses in macrophages. Activation of macrophages with lipopolysaccharide (LPS) elevates miR-155, while the anti-inflammatory cytokine interleukin-10 (IL10) reduces miR-155 levels. MiR-155 exists in two forms, miR-155-5p and miR-155-3p, produced from the precursor of miR-155 (pre-miR-155). MiR-155-5p is the most abundant strand in activated macrophages, but in response to LPS, the miR-155-3p level is upregulated first, followed by miR-155-5p later. We have previously identified CELF2 protein which interacts with pre-miR-155 and impairs miR-155-5p expression. We now show that CELF2 only regulates the miR-155-5p expression and that another protein FUBP1 controls miR-155-3p levels in response to LPS and IL10.

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