Interleukin-10 is a protective factor against diet-induced insulin resistance in liver

Cintra, Dennys E.; Pauli, José Rodrigo; Araújo, Eliana P.; Moraes, João Carlos Silos; Souza, Cláudio Teodoro de; Milanski, Marciane; Morari, Joseane; Gambero, Alessandra; Saad, Mário José Abdalla; Velloso, Lı́cio A.

doi:10.1016/j.jhep.2007.12.017

Cited by 158 publications

(157 citation statements)

References 44 publications

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“…In agreement with the well-known immunomodulatory activity of IL-10 in several tissues, several studies have reported a role for IL-10 as a protective cytokine against hepatic injury in diseases such as diet-induced insulin resistance in liver (Cintra et al, 2008), experimental hepatitis induced by LPS (Santucci et al, 1996) and concanavalin A (Louis et al, 1997), schistosomiasis (Winn et al, 1998), alcoholic hepatitis (Le Moine et al, 1995), hepatitis C virus infection (Kaplan et al, 2008) and fatty liver disease (Den Boer et al, 2006). The immunosuppressive cytokine IL-10 is crucial for tolerance induction in concanavalin A-induced liver damage in mice and is mainly expressed by CD4 + CD25 + regulatory T cells (Erhardt et al, 2007).…”

Section: The Antiinflammatory Cytokine Il-10 Is Regulated By Nf-kb1 (supporting

confidence: 69%

NF‐κB in liver diseases: a target for drug therapy

Muriel

2008

J of Applied Toxicology

148

106

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There are five nuclear factor-kB (NF-kB) transcription factors with important roles in innate immunity, liver inflammation, fibrosis and apoptosis prevention. Several inhibitors of NF-kB, like caffeic acid, captopril, curcumin, pyrrolidine dithiocarbamate, resveratrol, silymarin and thalidomide, have demonstrated antinecrotic, anticholestatic, antifibrotic and anticancer activities in the liver. A link between inflammation and hepatocellular carcinoma through the NF-kB pathway has been observed, providing ample experimental support for the tumor-promoting function of NF-kB in various models of cancer. NF-kB has been associated with the induction of proinflammatory gene expression and has attracted interest as a target for the treatment of inflammatory disease. However, despite much attention being focused on the deleterious effects of NF-kB, activation of this factor during the resolution of inflammation is associated with the production of antiinflammatory molecules like interleukin (IL)-10 and the onset of apoptosis. This suggests that NF-kB has an antiinflammatory role in vivo involving the regulation of the resolution of inflammation. Also, NF-kB promotes liver regeneration by upregulating IL-6 and other molecules like hepatocyte growth factor. It has been postulated that the beneficial properties of NF-kB are due to p50 homodimers, whose activation prevents cholestatic and chronic liver injury. More basic understanding on the function of the diverse NF-kB factors is urgently needed in different physiological and pathological conditions, because depending on the subunit composition of the dimmer, the disease and the stage of the illness, inhibition of the factor may result in a beneficial or in a deleterious response. Copyright © 2008 John Wiley & Sons, Ltd.There are five nuclear factor-kB (NF-kB) transcription factors with important roles in innate immunity, liver inflammation, fibrosis, and apoptosis prevention. Several inhibitors of NF-kB have demonstrated antinecrotic, anticholestatic, antifibrotic and anticancer activities in the

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Section: The Antiinflammatory Cytokine Il-10 Is Regulated By Nf-kb1 (supporting

confidence: 69%

NF‐κB in liver diseases: a target for drug therapy

Muriel

2008

J of Applied Toxicology

148

106

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“…Although the role of IL-10 in obesity-induced inflammation and liver disease is not fully elucidated, macrophages in the adipose tissue of mice fed a high-fat diet undergo a phenotypic switch from IL-10-producing M2 macrophages to TNF␣-producing M1 macrophages (44), and the latter are directly linked with insulin resistance (45). Furthermore, mice lacking IL-10 demonstrate more severe liver inflammation and steatosis following a highfat diet (46,47), suggesting that IL-10 may play a protective role in NAFLD.…”

Section: Discussionmentioning

confidence: 99%

Bile Acid Receptor Activation Modulates Hepatic Monocyte Activity and Improves Nonalcoholic Fatty Liver Disease

McMahan

Wang

Cheng

et al. 2013

Journal of Biological Chemistry

200

146

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Background:The bile acid receptors FXR and TGR5 have pleiotropic functions, including immune modulation. Results: Treatment of a murine model of nonalcoholic fatty liver disease (NAFLD) with a dual FXR/TGR5 agonist decreased intrahepatic inflammation and altered the immune phenotype of monocytes. Conclusion: Bile acid receptor activation improves NAFLD. Significance: These results identify potential targeting strategies for treatment of NAFLD.

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“…Also, in our study a highly significant negative correlation between TNF-a and IL-10 in both NASH and fibrosis groups was found and the correlation increases by progression of liver disease where IL-10 secretion inhibited and increases in serum TNF-a concentrations were found. Treatment with IL-10 could significantly reduce TNF-a mRNA expression in the liver after administration of the toxins to sensitized mice [37][38][39]. These findings suggest that IL-10 is capable of regulating hepatic injury in vivo mediated by T cells and macrophages [34] thus it hypothesized that high IL-10 levels limiting the effects of the inflammatory response that is, by counter regulating the effects of pro-inflammatory cytokine so that the protective function of IL-10 in steatotic liver relies on suppression of TNF-a production [40].…”

Section: Discussionmentioning

confidence: 99%