Dietary fatty acids modulate antigen presentation to hepatic NKT cells in nonalcoholic fatty liver disease

Hua, Jing; Ma, Xiong; Webb, Tonya J.; Potter, James J.; Oelke, Mathias; Li, Zhiping

doi:10.1194/jlr.m003004

Cited by 43 publications

(41 citation statements)

References 38 publications

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“…We established a long term HF diet-induced NAFLD mice model2930. As previously reported, long term HF diet induced hepatic steatosis and significantly increased hepatic expression of pro-inflammatory cytokines in HF diet-fed mice (Fig.…”

Section: Resultsmentioning

confidence: 87%

Effect of modulation of PPAR-γ activity on Kupffer cells M1/M2 polarization in the development of non-alcoholic fatty liver disease

Luo¹,

Xu²,

Wang³

et al. 2017

Sci Rep

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203

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Abnormal lipid-mediated hepatic inflammatory-immune dysfunction and chronic low grade inflammation play an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Macrophage polarization is an important mechanism for the regulation of inflammatory response. Since PPAR-γ has emerged as a master regulator of macrophage polarization, we aimed to investigate the lipid-induced macrophage/Kupffer cell polarization in vivo and in vitro, and explore the association between PPAR-γ activity and macrophages M1/M2 polarization shifting. Here we showed that long-term high-fat diet increased Kupffer cells content with M1-predominant phenotype and increasing production of pro-inflammatory cytokines. Saturated fatty acids polarized Kupffer cells/macrophages to an M1-predominant phenotype while n-3 PUFA polarized Kupffer cells/macrophages to an M2 phenotype, which was associated with activation of NF-κB signal pathway and PPAR-γ respectively. Furthermore, up-regulation of PPAR-γ shifted lipid-induced macrophages polarization from M1-predominant phenotype to M2 phenotype. Macrophages polarization switch was associated with the interaction between PPAR-γ and NF-κBp65 signal pathway. Rosiglitazone restored high-fat diet-induced imblance of Kupffer cells M1/M2 polarization and alleviated hepatic steatosis as well as local pro-inflammatory response. These findings suggest that manipulation of PPAR-γ activity has the potential to balance lipid-induced M1/M2 macrophage/Kupffer cell polarization, and leading to prevent the development of NAFLD.

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Section: Resultsmentioning

confidence: 87%

Effect of modulation of PPAR-γ activity on Kupffer cells M1/M2 polarization in the development of non-alcoholic fatty liver disease

Luo¹,

Xu²,

Wang³

et al. 2017

Sci Rep

Self Cite

203

166

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“…Once activated, iNKT cells function as immune orchestrators by participating in bidirectional activation with antigen presenting cells and by transactivation of other effector leukocytes. Here, we have highlighted examples of crosstalk with Kupffer cells (Lee et al 2010), DCs (Arora et al 2014; Bai et al 2012; Brigl et al 2003; Cohen et al 2011; Tyznik et al 2008), MDSCs, CD8 + T cells (De Santo et al 2008), macrophage populations (Barral et al 2010; Kawakami et al 2003; Lee et al 2010; Nieuwenhuis et al 2002), and non-hematopoietic cells (Hua et al 2010; Huh et al 2013; Olszak et al 2014; Rakhshandehroo et al 2014; Satoh et al 2016; Zeissig et al 2012). In other examples that were not discussed here, iNKT cells have been shown to activate or modulate the function of granulocytes (De Santo et al 2010), B cells (Chang et al 2012; Galli et al 2007; King et al 2012; Leadbetter et al 2008), adaptive T cells (Fujii et al 2004; Hermans et al 2003), and NK cells (Carnaud et al 1999; Schmieg et al 2003).…”

Section: Discussionmentioning

confidence: 98%

“…By selective ablation of CD1d from intestinal epithelium using a transgenic mouse approach, Olszak and colleagues showed that ligation of CD1d in the gut epithelium by tissue-resident iNKT cells induced IL-10 expression in intestinal epithelial cells, providing protection in a model of colitis (Olszak et al 2014). Hepatocytes also express CD1d and have been implicated in iNKT cell activation in multiple contexts (Hua et al 2010; Zeissig et al 2012). …”

Section: Lipid Uptake and Presentation By Cd1dmentioning

confidence: 99%

Activation strategies for invariant natural killer T cells

et al. 2016

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Invariant natural killer T (iNKT) cells are a specialized T cell subset that plays an important role in host defense, orchestrating both innate and adaptive immune effector responses against a variety of microbes. Specific microbial lipids and mammalian self lipids displayed by the antigen-presenting molecule CD1d can activate iNKT cells through their semi-invariant αβ T cell receptors (TCRs). iNKT cells also constitutively express receptors for inflammatory cytokines typically secreted by antigen-presenting cells (APCs) after recognition of pathogen-associated molecular patterns (PAMPs), and they can be activated through these cytokine receptors either in combination with TCR signals, or in some cases even in the absence of TCR signaling. During infection, experimental evidence suggests that both TCR-driven and cytokine-driven mechanisms contribute to iNKT cell activation. While the relative contributions of these two signaling mechanisms can vary widely depending on the infectious context, both lipid antigens and PAMPs mediate reciprocal activation of iNKT cells and APCs, leading to downstream activation of multiple other immune cell types to promote pathogen clearance. In this review, we discuss the mechanisms involved in iNKT cell activation during infection, focusing on the central contributions of both lipid antigens and PAMP-induced inflammatory cytokines, and highlight in vivo examples of activation during bacterial, viral, and fungal infections.

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“…"It has been showed that specific nutritional elements can affect performance of immune system [4][5][6]". "It is interesting that some metabolites can shift immune response by their effects on differentiation of Th cells [7][8][9][10][11][12][13][14]".…”

Section: Introductionmentioning

confidence: 99%

Fatty Acids Effect on T Helper Differentiation in Vitro

zade¹,

Moogooei²,

Mostafaei³

et al. 2016

IJNFS

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Autoimmunity shows a concerning growth recently. It seems that role of diet is important for development of autoimmunity. Nutritional elements can affect immune system functions. Oversupply or deficiency of specific metabolites may change performance of immune cells, especially that of T helper lymphocytes. For example, glucose, omega 3 and poly unsaturated fatty acids can induce specific Th subsets which play a critical role in autoimmune diseases. T lymphocytes, mostly T CD4 + (Th cells) not only play a critical role in orchestrating immune responses, but also they have major role in pathogenesis of some autoimmune disease. Hence, we designed a research to find out effects of oleic and palmitic acids on differentiation of Th cells. We added oleic acid, palmitic acids and combination of them on peripheral blood mononuclear cells (PBMC) culture and cells were harvested for RT-PCR and flow cytometry analysis after seven days. Our results showed that palmitic and oleic acids induce Th1 and Th17 subsets (p-valu<0.05).

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Dietary fatty acids modulate antigen presentation to hepatic NKT cells in nonalcoholic fatty liver disease

Cited by 43 publications

References 38 publications

Effect of modulation of PPAR-γ activity on Kupffer cells M1/M2 polarization in the development of non-alcoholic fatty liver disease

Effect of modulation of PPAR-γ activity on Kupffer cells M1/M2 polarization in the development of non-alcoholic fatty liver disease

Activation strategies for invariant natural killer T cells

Fatty Acids Effect on T Helper Differentiation in Vitro

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