Hepatic Macrophages are the Cell Source of Hepatic Procalcitonin in Acute Liver Failure
Hepatic Macrophages are the Cell Source of Hepatic Procalcitonin in Acute Liver Failure
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肝巨噬细胞是急性肝衰竭中肝降钙素原的细胞来源
DOI：
10.1159/000490207
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发表时间：
2018-06
期刊：
影响因子：
--
通讯作者：
Min Zheng
中科院分区：
文献类型：
--
作者：
Weiyang Zheng;Bingjue Ye;Xue Liang;Liyan Shui;Guohua Lou;Yanning Liu;Min Zheng
背景/目的：血清降钙素原（PCT）在急性肝衰竭（ALF）中升高，但PCT在肝脏中的表达尚未阐明。本研究旨在阐明肝纤维化中PCT表达的调控及其细胞来源。研究方法：用12-O-十四酰基佛波醇-13-乙酸酯（PMA）（100 ng/ mL）处理人单核细胞白血病系U937细胞24 h以诱导活化的巨噬细胞。在脂多糖（LPS，1 μg/mL）存在下，活化的巨噬细胞与人肝细胞系L02细胞共同孵育或共培养0、2、6和24 h。在体内实验中，雄性C57 BL/6小鼠用腹膜内LPS/D-半乳糖胺（LPS/D-GalN）攻击。采用全自动生化分析仪测定血清丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）。采用实时荧光定量PCR检测炎症介质，采用苏木精-伊红（HE）染色和免疫组织化学（IHC）检测肝脏组织学。结果：LPS可诱导U937激活的巨噬细胞PCT mRNA表达上调，但对L02细胞无明显影响。当与L02细胞共培养时，与对照相比，活化的巨噬细胞的PCT mRNA的表达上调;然而，在LPS存在下，活化的巨噬细胞不诱导L02细胞中PCT mRNA的表达。此外，在LPS/D-GalN攻击的ALF小鼠模型中，血清肝酶（ALT、AST）、炎症、坏死和PCT的肝表达显著升高。免疫组化显示PCT表达与肝巨噬细胞共定位。结论：ALF时肝PCT表达上调。肝巨噬细胞而不是肝细胞是肝PCT表达的细胞来源。
Background/Aims: Serum procalcitonin (PCT) is elevated in acute liver failure (ALF), but the expression of PCT in the liver has not been elucidated. We aimed to clarify the regulation of hepatic PCT expression and the cell sources in ALF. Methods: Human monocytic leukemia line U937 cells were treated with 12-O-tetradecanoylphorbol-l3-acetate (PMA) (100 ng/ mL) for 24 h to induce activated macrophages. In the presence of lipopolysaccharide (LPS, 1 μg/mL), activated macrophages and human hepatocyte line L02 cells were incubated with LPS or co-cultured for 0, 2, 6, and 24 h. In an in vivo experiment, male C57BL/6 mice were challenged with intraperitoneal LPS/D-galactosamine (LPS/D-GalN). Serum liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured using an automatic chemical analyzer. Inflammatory mediators were measured by real-time PCR and liver histology was examined by hematoxylin-eosin (HE) staining and immunohistochemistry (IHC). Results: LPS induced the upregulation of PCT mRNA in U937-activated macrophages but not in L02 cells. When co-cultured with L02 cells, the expression of PCT mRNA of activated macrophages was upregulated compared to controls; however, the activated macrophages did not induce the expression of PCT mRNA in L02 cells in the presence of LPS. Moreover, serum liver enzymes (ALT, AST), inflammation, necrosis, and hepatic expression of PCT were significantly elevated in the LPS/D-GalN-challenged ALF mouse model. IHC revealed that PCT expression was co-localized with hepatic macrophages. Conclusions: Hepatic PCT expression is upregulated in ALF. Hepatic macrophages but not hepatocytes are the cell source of hepatic PCT expression.
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影响因子：
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作者：
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影响因子：
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作者：
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1
作者：
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影响因子：
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作者：
Meisner, M;Müller, V;Redl, H
通讯作者：
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DOI：
--
发表时间：
2016-04
期刊：
The new microbiologica
影响因子：
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作者：
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通讯作者：
A. Sbrana;M. Torchio;G. Comolli;A. Antonuzzo;M. Danova