Effects of macrophage depletion on the induction of histidine decarboxylase by lipopolysaccharide, interleukin 1 and tumour necrosis factor

Effects of macrophage depletion on the induction of histidine decarboxylase by lipopolysaccharide, interleukin 1 and tumour necrosis factor
复制标题

巨噬细胞耗竭对脂多糖、白细胞介素 1 和肿瘤坏死因子诱导组氨酸脱羧酶的影响

DOI:
--
复制
发表时间:
1995
影响因子:
7.3
通讯作者:
K. Kumagai
K. Kumagai
中科院分区:
医学2区
文献类型:
--
作者:
Y. Endo;M. Nakamura;Y. Nitta;K. Kumagai

文献摘要

参考文献

被引文献

相似文献

1我们以前的工作表明,向小鼠注射脂多糖(LPS)和细胞因子白细胞介素1(IL-1)和肿瘤坏死因子(TNF)可诱导组氨酸脱羧酶(HDC),这是一种形成组胺的酶,在各种组织中,如肝,肺,脾和骨髓,但不在血液中。HDC的诱导也发生在裸鼠和肥大细胞缺陷小鼠中。另一方面,造血细胞因子如IL-3、粒细胞集落刺激因子(G-CSF)和粒细胞-巨噬细胞CSF(GM-CSF)仅在造血器官(即骨髓和脾脏)中诱导HDC。在本研究中,检查了巨噬细胞耗竭对HDC诱导的影响。2在单次静脉注射巨噬细胞消耗剂(包封二氯亚甲基二膦酸盐的脂质体,当摄入巨噬细胞时是有毒的)后的第1天,肝脏中的巨噬细胞几乎完全消耗,脾脏和骨髓中的巨噬细胞减少约50%,但肺中的巨噬细胞没有受到显著影响。在第3天,消耗程度与第1天相似。在脾脏中,红髓中的巨噬细胞耗尽,并且存在结构破坏。3在巨噬细胞耗竭的小鼠中,LPS、IL-1α或TNF-α诱导的HDC在肝脏中未受损,在肺和骨髓中增强。在第3天,HDC的诱导仅在脾脏中减少。4LPS不能诱导成年大鼠脾脏中的HDC,其相应地在造血中是无活性的。5这些结果表明,响应于LPS、IL-1和TNF诱导HDC活性的主要细胞不是循环粒细胞、循环单核细胞、来源于胸腺的T细胞、肥大细胞或吞噬巨噬细胞。基于这些结果,我们讨论了在非造血器官和造血器官中诱导HDC的主要细胞分别是内皮细胞和造血前体细胞的可能性。
1 Our previous work has shown that injection into mice of lipopolysaccharide (LPS) and the cytokines interleukin 1 (IL‐1) and tumour necrosis factor (TNF) induces histidine decarboxylase (HDC), the enzyme forming histamine, in various tissues such as liver, lung, spleen and bone marrow, but not in the blood. The induction of HDC also occurs in nude mice and mast cell‐deficient mice. On the other hand, haematopoietic cytokines such as IL‐3, granulocyte colony‐stimulating factor (G‐CSF) and granulocyte – macrophage CSF (GM‐CSF) only induce HDC in the haematopoietic organs, i.e. bone marrow and spleen. In the present study, the effect of macrophage depletion on the induction of HDC was examined. 2 On day 1 after a single intravenous injection of a macrophage depletor (liposomes encapsulating dichloromethylene diphosphonate, which is toxic when ingested into macrophages), macrophages were almost completely depleted in the liver and reduced by about 50% in the spleen and bone marrow, but not significantly affected in the lung. On day 3, the degrees of the depletion were similar to those of day 1. In the spleen, macrophages were depleted in the red pulp, and there was a structural destruction. 3 In macrophage‐depleted mice, the induction of HDC by LPS, IL‐1α or TNF‐α was not impaired in the liver, and was potentiated in the lung and bone marrow. The induction of HDC was decreased only in the spleen at day 3. 4 HDC was not induced by LPS in the spleen of the adult rat, which is correspondingly inactive in haematopoiesis. 5 These results indicate that the major cells in which HDC activity is induced in response to LPS, IL‐1 and TNF are not circulating granulocytes, circulating monocytes, T cells derived from thymus, mast cells or phagocytic macrophages. Based on these results, we discuss the possibility that the major cells in which HDC was induced in non‐haematopoietic and haematopoietic organs were endothelial cells and haematopoietic precursor cells respectively.
DOI: 10.1182/blood.v77.8.1627.bloodjournal7781627
发表时间: 1991-04
期刊: Blood
影响因子: 20.3
作者:
C. Dinarello
通讯作者: C. Dinarello
内毒素休克的内源性介质。
DOI: --
发表时间: 1987
期刊: Clinical research
影响因子: --
作者:
Beutler,B;Cerami,A
通讯作者: Cerami,A