Literature DB >> 19708080

Immature myeloid cells induced by a high-fat diet contribute to liver inflammation.

Zhong-bin Deng1, Yuelong Liu, Cunren Liu, Xiaoyu Xiang, Jianhua Wang, Ziqiang Cheng, Spandan V Shah, Shuangyin Zhang, Liming Zhang, Xiaoying Zhuang, Sue Michalek, William E Grizzle, Huang-Ge Zhang.   

Abstract

UNLABELLED: Chronic inflammation plays a critical role in promoting obesity-related disorders, such as fatty liver disease. The inflammatory cells that mediate these effects remain unknown. This study investigated the accumulation of immature myeloid cells in the liver and their role in liver inflammation. We found that the accumulation of immature myeloid cells, i.e., CD11b(+)Ly6C(hi)Ly6G(-) cells, in the liver of B6 mice fed a high-fat diet contribute to liver inflammation. Adoptive transfer of CD11b(+)Ly6C(hi)Ly6G(-) cells isolated from the liver of obese B6 mice, but not from lean B6 mice, resulted in liver damage that was evident by an increase in the activity of liver transferases in serum. CD11b(+)Ly6C(hi)Ly6G(-) cells isolated from the liver of obese mice are more easily activated by way of Toll-like receptor (TLR) stimulation resulting in interleukin 12 and other inflammatory cytokine expression in an MyD88-dependent fashion. TLR7-activated CD11b(+)Ly6C(hi)Ly6G(-) cells also enhance liver natural killer T cell (NKT) death in an Fas-dependent manner. Experiments using mice depleted of Gr-1(+) immature myeloid cells demonstrated the important role of CD11b(+)Ly6C(hi)Ly6G(-) in liver inflammation. Repeated injection of exosome-like particles causes CD11b(+) cell activation and subsequent homing to and accumulation of the cells in the liver.
CONCLUSION: Consumption of a high-fat diet by B6 mice triggers an accumulation of immature myeloid cells in the liver. The immature myeloid cells release proinflammatory cytokines and induce NKT cell apoptosis. Activation-induced NKT apoptosis further promotes excessive production of Th-1 cytokines. This diet-induced accumulation of immature myeloid cells may contribute to obesity-related liver disease.

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Year:  2009        PMID: 19708080      PMCID: PMC2852608          DOI: 10.1002/hep.23148

Source DB:  PubMed          Journal:  Hepatology        ISSN: 0270-9139            Impact factor:   17.425


  21 in total

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4.  Dietary factors alter hepatic innate immune system in mice with nonalcoholic fatty liver disease.

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Journal:  Hepatology       Date:  2005-10       Impact factor: 17.425

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8.  Tumor exosomes inhibit differentiation of bone marrow dendritic cells.

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9.  Obese and diabetic db/db mice develop marked liver fibrosis in a model of nonalcoholic steatohepatitis: role of short-form leptin receptors and osteopontin.

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10.  MyD88-dependent expansion of an immature GR-1(+)CD11b(+) population induces T cell suppression and Th2 polarization in sepsis.

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  66 in total

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Review 3.  Roles of liver innate immune cells in nonalcoholic fatty liver disease.

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4.  Expression of STING Is Increased in Liver Tissues From Patients With NAFLD and Promotes Macrophage-Mediated Hepatic Inflammation and Fibrosis in Mice.

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Review 6.  Exosomes: new molecular targets of diseases.

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Review 8.  Extracellular vesicles in liver pathobiology: Small particles with big impact.

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9.  Transcriptional profiles of leukocyte populations provide a tool for interpreting gene expression patterns associated with high fat diet in mice.

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Journal:  PLoS One       Date:  2010-07-29       Impact factor: 3.240

10.  C-C chemokine receptor 2 (CCR2) regulates the hepatic recruitment of myeloid cells that promote obesity-induced hepatic steatosis.

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