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首页> 外文期刊>The journal of immunology >S100A8 Production in CXCR2-Expressing CD11b+Gr-1high Cells Aggravates Hepatitis in Mice Fed a High-Fat and High-Cholesterol Diet
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S100A8 Production in CXCR2-Expressing CD11b+Gr-1high Cells Aggravates Hepatitis in Mice Fed a High-Fat and High-Cholesterol Diet

机译：在高脂高胆固醇饮食喂养的小鼠中，表达CXCR2的CD11b + Gr-1high细胞产生S100A8加重肝炎

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Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease with a spectrum of presentations. S100A8 has been suggested to play a pivotal role as an endogenous immune-activator in inflammatory diseases. In this study, we investigated the involvement of S100A8 in the development of NAFLD. We used a diet model of NAFLD, in which mice were fed either a high-fat and high-cholesterol diet (HFHCD) or a normal diet (ND) as a control. We also assessed liver tissues from patients with NAFLD, including patients with nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). HFHCD-fed mice, but not ND-fed mice, developed steatohepatitis. S100A8 expression was significantly elevated in the livers of HFHCD-fed mice compared with the controls. S100A8 was exclusively expressed in CXCR2-expressing CD11b+Gr-1high cells, which significantly increased in the livers of HFHCD-fed mice. These cells were F4/80 negative and did not possess a suppressor function. TNF-α expression was enhanced by S100A8 in primary liver leukocytes or a hepatocyte cell line and significantly elevated in the livers of HFHCD-fed mice. TNF-α was primarily produced from CD11b+F4/80+ cells in liver leukocytes in response to S100A8. TNF-α deficiency attenuated hepatitis in HFHCD-fed mice. S100A8 was significantly more expressed in the liver tissues of patients with NASH than in those of patients with NAFL. In conclusion, these results suggest that S100A8 is primarily produced from CXCR2-expressing CD11b+Gr-1high cells, and it upregulates TNF-α production in CD11b+F4/80+ cells through cellular cross-talk, which is an important mechanism in the development of NAFLD.
机译：非酒精性脂肪性肝病（NAFLD）是一种常见的慢性肝病，具有多种表现形式。已建议在炎症性疾病中S100A8作为内源性免疫激活剂发挥关键作用。在这项研究中，我们调查了S100A8在NAFLD发育中的参与。我们使用了NAFLD的饮食模型，其中以高脂高胆固醇饮食（HFHCD）或正常饮食（ND）喂养小鼠。我们还评估了NAFLD患者的肝组织，包括非酒精性脂肪肝（NAFL）和非酒精性脂肪性肝炎（NASH）的患者。 HFHCD喂养的小鼠而非ND喂养的小鼠发展为脂肪性肝炎。与对照组相比，HFHCD喂养的小鼠肝脏中的S100A8表达显着升高。 S100A8仅在表达CXCR2的CD11b + Gr-1high细胞中表达，在以HFHCD喂养的小鼠的肝脏中显着增加。这些细胞是F4 / 80阴性的，不具有抑制功能。 S100A8在原代肝白细胞或肝细胞系中增强了TNF-α的表达，而在HFHCD喂养的小鼠的肝脏中，TNF-α的表达则明显升高。响应于S100A8，TNF-α主要由肝白细胞中的CD11b + F4 / 80 +细胞产生。 TNF-α缺乏可减轻HFHCD喂养小鼠的肝炎。与NAFL患者相比，S100A8在NASH患者的肝组织中表达更高。总之，这些结果表明，S100A8主要是由表达CXCR2的CD11b + Gr-1high细胞产生的，并且它通过细胞串扰上调CD11b + F4 / 80 +细胞中TNF-α的产生，这是产生S100A8的重要机制。 NAFLD的发展。

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