Earlier onset of neutrophil-mediated inflammation in the ultraviolet-exposed skin of mice deficient in myeloperoxidase and NADPH oxidase
Earlier onset of neutrophil-mediated inflammation in the ultraviolet-exposed skin of mice deficient in myeloperoxidase and NADPH oxidase
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DOI：
10.1007/s00011-006-0071-3
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发表时间：
2006-05-01
影响因子：
6.7
通讯作者：
Aratani, Y.
中科院分区：
文献类型：
--
作者：
Komatsu, J.;Koyama, H.;Aratani, Y.
目标和设计：本研究探讨了嗜中性粒细胞衍生的活性氧（ROS）在紫外线B（UVB）照射小鼠皮肤后中性粒细胞聚集中的作用。组织化学观察到炎症部位内中性粒细胞的积聚。角质形成细胞衍生的趋化因子（KC）和巨噬细胞炎性蛋白2（MIP-2）进行了定量，并在体内对KC和MIP-2的中性粒细胞的趋化性examined.Results：UVB暴露的小鼠髓过氧化物酶（MPO），NADPH氧化酶，或两者都缺乏，导致皮肤中性粒细胞浸润峰值分别在60，48和48小时，这是早于野生型小鼠的72小时的峰值。突变小鼠MIP-2水平高于野生型小鼠。突变型中性粒细胞在体外产生更多的MIP-2。突变体小鼠向KC局部来源的神经元迁移高于野生型小鼠。结论：中性粒细胞产生的活性氧调节MIP-2的表达和中性粒细胞向KC的迁移。这可能解释了突变型中性粒细胞对UVB的早期浸润。
Objective and design: This study examined the role of neutrophil-derived reactive oxygen species (ROS) in neutrophil recruitment into ultraviolet B (UVB)-exposed skin of mice.Methods: Mouse dorsal skin was irradiated with UVB (600mJ/cm(2)). 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.Results: 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 wildtype mice. NADPH oxidase deficiency had a greater effect on migration than MPO deficiency.Conclusions: 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.