scholarly journals ABIN-3: a Molecular Basis for Species Divergence in Interleukin-10-Induced Anti-Inflammatory Actions

2007 ◽  
Vol 27 (13) ◽  
pp. 4603-4616 ◽  
Author(s):  
Brian K. Weaver ◽  
Erwin Bohn ◽  
Barbi A. Judd ◽  
M. Pilar Gil ◽  
Robert D. Schreiber
Keyword(s):  
Macrophage Activation ◽  
Interleukin 10 ◽  
Mononuclear Phagocytes ◽  
Toll Like Receptor ◽  
Monocytic Cells ◽  
Proinflammatory Responses ◽  
Anti Inflammatory ◽  
Species Specific ◽  
Anti Inflammatory Cytokine ◽  
Necrosis Factor

ABSTRACT Whereas interleukin-10 (IL-10) is an anti-inflammatory cytokine known to regulate macrophage activation, its full mechanism of action remains incompletely defined. In a screen to identify novel IL-10-induced genes, we cloned the mouse ortholog of human ABIN-3 (also termed LIND). ABIN-3 expression was induced selectively by IL-10 in both mouse and human mononuclear phagocytes coordinately undergoing proinflammatory responses. In contrast to the previously characterized ABINs, mouse ABIN-3 was incapable of inhibiting NF-κB activation by proinflammatory stimuli. Generation and analysis of ABIN-3-null mice demonstrated that ABIN-3 is unnecessary for the anti-inflammatory effects of IL-10 as well as for proper negative regulation of NF-κB. Conversely, human ABIN-3 was capable of inhibiting NF-κB activation in response to signaling from Toll-like receptor, IL-1, and tumor necrosis factor. Enforced expression of human ABIN-3 in human monocytic cells suppressed the cytoplasmic degradation of IκBα, the activation of NF-κB, and the induction of proinflammatory genes. Comparative sequence analyses revealed that mouse ABIN-3 lacks a complete ABIN homology domain, which was required for the functional activity of human ABIN-3. ABIN-3 is, thus, an IL-10-induced gene product capable of attenuating NF-κB in human macrophages yet is inoperative in mice and represents a basis for species-specific differences in IL-10 actions.

scholarly journals Local and systemic influence of toxic levels of airborne ozone on the inflammatory response in rats

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Małgorzata Chmielewska-Krzesińska ◽  
Krzysztof Wąsowicz
Keyword(s):  
Inflammatory Response ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Interleukin 1 ◽  
Interleukin 10 ◽  
Necrosis Factor Alpha ◽  
Genes Expression ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Necrosis Factor

Abstract Introduction Ozone is not harmful itself; however, it directly oxidises biomolecules and produces radical-dependent cytotoxicity. Exposure to ozone is by inhalation and therefore the lungs develop the main anti-inflammatory response, while ozone has an indirect impact on the other organs. This study investigated the local and systemic effects of the ozone-associated inflammatory response. Material and Methods Three groups each of 5 Wistar Han rats aged 6 months were exposed for 2h to airborne ozone at 0.5 ppm and a fourth identical group were unexposed controls. Sacrifice was at 3h after exposure for control rats and one experimental group and at 24 h and 48 h for the others. Lung and liver samples were evaluated for changes in expression of transforming growth factor beta 1, anti-inflammatory interleukin 10, pro-inflammatory tumour necrosis factor alpha and interleukin 1 beta and two nuclear factor kappa-light-chain-enhancer of B cells subunit genes. Total RNA was isolated from the samples in spin columns and cDNA was synthesised in an RT-PCR. Expression levels were compared to those of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and analysed statistically. Results All variables changed non-linearly over time comparing experimental groups to the control. Conspicuous expression changes in the subunit genes and cytokines were observed in both evaluated organs. Conclusion Locally and systemically, inflammation responses to ozone inhalation include regulation of certain genes’ expression. The mechanisms are unalike in lungs and liver but ozone exerts a similar effect in both organs. A broader range of variables influential on ozone response should be studied in the future.

Inhibition of endotoxin-induced lung inflammation by interleukin-10 gene transfer in mice

2000 ◽  
Vol 279 (5) ◽  
pp. L872-L877 ◽  
Author(s):  
Sujatha Dokka ◽  
Carl J. Malanga ◽  
Xianglin Shi ◽  
Fei Chen ◽  
Vincent Castranova ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Lung Inflammation ◽  
Transgene Expression ◽  
Tumor Necrosis ◽  
Interleukin 10 ◽  
Inhibitory Effect ◽  
Biologically Active ◽  
Tnf Α ◽  
Anti Inflammatory Cytokine ◽  
Necrosis Factor

Interleukin (IL)-10 is an anti-inflammatory cytokine that has great potential for use in the treatment of inflammatory and immune illnesses. In this study, gene transfer was used to induce IL-10 transgene expression in murine lungs for treatment of endotoxin-induced lung inflammation. Gene transfer was performed with a cytomegalovirus (CMV)-IL-10 plasmid with the aid of the liposomal agents LipofectAMINE and N-[1-(2,3-dioleoyl)propyl]- N, N, N-trimethylammonium methylsulfate (DOTAP). Administration of the endotoxin caused a marked increase in lung inflammation as indicated by increased tumor necrosis factor (TNF)-α release and neutrophil count. Pretreatment of the mice with IL-10 plasmid with and without LipofectAMINE had no inhibitory effect on lung inflammation and IL-10 transgene expression. LipofectAMINE by itself induced lung inflammation, an effect that was not observed with DOTAP. IL-10 plasmid when codelivered with DOTAP expressed biologically active IL-10 protein and caused a reduction in endotoxin-induced inflammation. Transgene expression was observed as early as 3 h after administration, peaked at 12 h, and declined thereafter. We conclude that IL-10 gene transfer is a feasible approach for the treatment of lung inflammation.

Toll-like Receptor-mediated Tumor Necrosis Factor and Interleukin-10 Production Differ during Systemic Inflammation

2003 ◽  
Vol 168 (2) ◽  
pp. 158-164 ◽  
Author(s):  
Minou Adib-Conquy ◽  
Pierre Moine ◽  
Karim Asehnoune ◽  
Alain Edouard ◽  
Terje Espevik ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Systemic Inflammation ◽  
Tumor Necrosis ◽  
Interleukin 10 ◽  
Toll Like Receptor ◽  
Necrosis Factor

scholarly journals 1,25(OH)2D3 Differently Affects Immunomodulatory Activities of Mesenchymal Stem Cells Depending on the Presence of TNF-α, IL-1β and IFN-γ

2019 ◽  
Vol 8 (12) ◽  
pp. 2211 ◽  
Author(s):  
Christian Behm ◽  
Alice Blufstein ◽  
Johannes Gahn ◽  
Barbara Kubin ◽  
Michael Nemec ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Inflammatory Cytokines ◽  
T Lymphocyte ◽  
T Lymphocyte Proliferation ◽  
Tnf Α ◽  
Ifn Γ ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine ◽  
Necrosis Factor

Periodontal ligament-derived mesenchymal stem cells (hPDLSCs) possess immunomodulatory abilities which are strongly enhanced by various inflammatory cytokines. Vitamin D3 has anti-inflammatory effects on hPDLSCs and immune cells. However, no study to date has directly compared the influence of 1,25(OH)2D3 on the immunomodulatory activities of hPDLSCs in the presence of different cytokines. In the present study, the effects of hPDLSCs treated with tumor necrosis factor (TNF)-α, interleukin (IL)-1β, or interferon (IFN)-γ in the presence of 1,25(OH)2D3 on the proliferation of allogenic CD4+ T lymphocyte or on the functional status of primary CD68+ macrophages were analyzed in coculture models. Additionally, the effects of 1,25(OH)2D3 on TNF-α-, IL-1β-, and IFN-γ-induced gene expression of some immunomodulatory factors in hPDLSCs were compared. Under coculture conditions, 1,25(OH)2D3 increased or decreased CD4+ T lymphocyte proliferation via hPDLSCs, depending on the cytokine. hPDLSCs primed with 1,25(OH)2D3 and different cytokines affected pro- and anti-inflammatory cytokine expression in macrophages variably, depending on the priming cytokine. With one exception, 1,25(OH)2D3 significantly reduced TNF-α-, IL-1β-, and IFN-γ-induced expression of all the investigated immunomediators in hPDLSCs, albeit to different extents. These results suggest that 1,25(OH)2D3 influences the immunomodulatory activities of hPDLSCs depending qualitatively and quantitatively on the presence of certain inflammatory cytokines.

Time course of pro- and anti-inflammatory cytokine levels in patients with burns—Prognostic value of interleukin-10

Burns ◽  
2010 ◽  
Vol 36 (4) ◽  
pp. 483-494 ◽  
Author(s):  
C. Csontos ◽  
V. Foldi ◽  
L. Pálinkas ◽  
L. Bogar ◽  
E. Röth ◽  
...  
Keyword(s):  
Prognostic Value ◽  
Inflammatory Cytokine ◽  
Time Course ◽  
Interleukin 10 ◽  
Cytokine Levels ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

Selective excretion of anti-inflammatory cytokine Interleukin-10 in a superantigen-inducing neonatal infectious disease

Cytokine ◽  
2009 ◽  
Vol 45 (1) ◽  
pp. 39-43 ◽  
Author(s):  
Naoto Takahashi ◽  
Hisaya Hasegawa ◽  
Mami Komiyama ◽  
Takehiro Ohki ◽  
Yukari Yada ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Inflammatory Cytokine ◽  
Interleukin 10 ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine
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