Marley S B, Hadley C L, Wakelin D
Department of Life Science, University of Nottingham, UK.
Clin Exp Immunol. 1995 Oct;102(1):224-8. doi: 10.1111/j.1365-2249.1995.tb06660.x.
Genetic variation of induced peritoneal neutrophilia in mice was accompanied by parallel variation in macrophage responses. The timing of the macrophage responses in high responder (C57B1/10) mice indicated a potential role for these cells in mediating the enhanced neutrophil response. However, adoptive transfer of inflammatory macrophages did not induce neutrophilia. Analysis of peritoneal cytokine levels in high and low responder mice further indicated that IL-1, IL-3, GM-CSF, G-CSF and interferon-gamma (IFN-gamma) were not involved in mediating the genetic variation observed. Exogenous tumour necrosis factor-alpha (TNF-alpha) was effective in inducing the high responder phenotype, despite the absence of detectable TNF-alpha in either peritoneal fluid or serum. A role for genetically determined differential expression of endothelial adhesion molecules in high and low responders is suggested.
小鼠诱导性腹膜嗜中性粒细胞增多的基因变异伴随着巨噬细胞反应的平行变异。高反应性（C57B1/10）小鼠中巨噬细胞反应的时间表明这些细胞在介导增强的嗜中性粒细胞反应中具有潜在作用。然而，炎性巨噬细胞的过继转移并未诱导嗜中性粒细胞增多。对高反应性和低反应性小鼠腹膜细胞因子水平的分析进一步表明，白细胞介素-1、白细胞介素-3、粒细胞-巨噬细胞集落刺激因子、粒细胞集落刺激因子和干扰素-γ不参与介导所观察到的基因变异。外源性肿瘤坏死因子-α可有效诱导高反应性表型，尽管在腹膜液或血清中均未检测到可检测到的肿瘤坏死因子-α。提示高反应性和低反应性小鼠中内皮黏附分子的基因决定差异表达具有作用。
