Suzuki M, Nakano K
Nagoya University Bioscience Center, Japan.
Biochem Pharmacol. 1996 Sep 13;52(5):809-13. doi: 10.1016/0006-2952(96)00342-5.
This study set out to examine the possible role of liver macrophages in histamine synthesis in the injured liver. The effects of the hepatotoxins Escherichia coli lipopolysaccharide (LPS) and CCl4 on histamine synthesis in the liver of mice were evaluated. C3H/HeJ mice were resistant to LPS in including histidine decarboxylase (HDC) in the liver compared with C3H/HeN mice and mast cell-deficient W/Wv mice. However, C3H/HeJ mice did respond strongly to another hepatotoxin, CCl4, leading to a significant increase in HDC activity. CCl4 also caused a marked increase in HDC activity and histamine levels in the liver of W/Wv mice. In addition, injection of CCl4 produced a large increase in the activity of HDC in the spleen and lung of W/Wv mice. HDC activity was confined to the nonparenchymal cells, with parenchymal cells expressing essentially no HDC activity. The CCl4-induced increase in HDC activity was confined, at least in part, to the liver macrophages. These results indicate that the macrophages are responsible for the increase in HDC-dependent histamine production in the liver caused by the injection of hepatotoxins. The possible role of histamine in liver regeneration after injury is discussed.
本研究旨在探讨肝巨噬细胞在受损肝脏组胺合成中可能发挥的作用。评估了肝毒素大肠杆菌脂多糖（LPS）和四氯化碳（CCl4）对小鼠肝脏组胺合成的影响。与C3H/HeN小鼠和肥大细胞缺陷型W/Wv小鼠相比，C3H/HeJ小鼠对LPS具有抗性，其肝脏中包括组氨酸脱羧酶（HDC）。然而，C3H/HeJ小鼠对另一种肝毒素CCl4反应强烈，导致HDC活性显著增加。CCl4还使W/Wv小鼠肝脏中的HDC活性和组胺水平显著升高。此外，注射CCl4使W/Wv小鼠脾脏和肺中的HDC活性大幅增加。HDC活性局限于非实质细胞，实质细胞基本不表达HDC活性。CCl4诱导的HDC活性增加至少部分局限于肝巨噬细胞。这些结果表明，巨噬细胞是注射肝毒素后肝脏中依赖HDC的组胺产生增加的原因。文中还讨论了组胺在损伤后肝脏再生中的可能作用。
