Komatsu J, Koyama H, Maeda N, Aratani Y
Kihara Institute for Biological Research, Yokohama City University, Maioka-cho 641-12, Totsuka, Yokohama, 244-0813, Japan.
Inflamm Res. 2006 May;55(5):200-6. doi: 10.1007/s00011-006-0071-3.
This study examined the role of neutrophil-derived reactive oxygen species (ROS) in neutrophil recruitment into ultraviolet B (UVB)-exposed skin of mice.
Mouse dorsal skin was irradiated with UVB (600 mJ/cm2). Accumulation of neutrophils within the inflammatory sites was observed histochemically. Keratinocyte-derived chemokine (KC) and macrophage inflammatory protein 2 (MIP-2) were quantified, and in vivo chemotaxis of neutrophils toward KC and MIP-2 was examined.
UVB exposure of mice deficient in myeloperoxidase (MPO), NADPH oxidase, or both, caused skin neutrophil infiltration peaking at 60, 48, and 48 h, respectively, which was earlier than the 72-h peak in wild-type mice. MIP-2 level was higher in mutant than wild-type mice. Mutant neutrophils produced more MIP-2 in vitro. Neutrophil migration toward a localized source of KC was higher in mutant than wild type mice. NADPH oxidase deficiency had a greater effect on migration than MPO deficiency.
These results suggest that ROS produced by neutrophils regulate expression of MIP-2 and migration of neutrophils toward KC. This may explain the earlier infiltration of mutant neutrophils in response to UVB.
本研究检测了中性粒细胞衍生的活性氧（ROS）在中性粒细胞募集至紫外线B（UVB）照射的小鼠皮肤中的作用。
用UVB（600 mJ/cm²）照射小鼠背部皮肤。通过组织化学方法观察炎症部位中性粒细胞的聚集情况。对角质形成细胞衍生趋化因子（KC）和巨噬细胞炎性蛋白2（MIP-2）进行定量，并检测中性粒细胞对KC和MIP-2的体内趋化性。
髓过氧化物酶（MPO）缺陷、NADPH氧化酶缺陷或两者均缺陷的小鼠经UVB照射后，皮肤中性粒细胞浸润分别在60、48和48小时达到峰值，早于野生型小鼠的72小时峰值。突变小鼠的MIP-2水平高于野生型小鼠。突变的中性粒细胞在体外产生更多的MIP-2。突变小鼠中性粒细胞向局部KC来源的迁移高于野生型小鼠。NADPH氧化酶缺陷对迁移的影响大于MPO缺陷。
这些结果表明，中性粒细胞产生的ROS调节MIP-2的表达以及中性粒细胞向KC的迁移。这可能解释了突变的中性粒细胞对UVB反应时更早的浸润现象。
