Alopecia in IL-10-deficient mouse pups is c-kit-dependent and can be triggered by iron deficiency.
Alopecia in IL-10-deficient mouse pups is c-kit-dependent and can be triggered by iron deficiency.
复制标题
IL-10 缺陷小鼠幼崽的脱发是 c-kit 依赖性的，并且可由缺铁引发。
DOI：
10.1111/j.1600-0625.2009.01032.x
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发表时间：
2010
影响因子：
3.6
通讯作者：
Hale,LauraP
中科院分区：
文献类型：
--
作者：
Vanderford,DeborahA;Greer,PaulaK;Sharp,JulieM;Chichlowski,Maciej;Rouse,DClayburn;Selim,MAngelica;Hale,LauraP
请引用这篇论文：IL-10缺陷小鼠的脱发是c-kit依赖的，并可由缺铁引发。实验皮肤病2010；19：518-526。摘要：脱发可由多种代谢、内分泌、免疫和环境因素引起。本研究旨在探讨C57BL/6白介素10基因缺陷(IL10-−/−)小鼠窝内散发性脱发的发病机制。所有受影响的幼崽在出生后17-19天都表现出脱发，躯干脱发，但头部、尾巴底部或脚没有脱发。组织病理学显示扭曲的毛囊含有断裂的毛干和明显的真皮浸润物，含有大量激活的肥大细胞。断奶后不久，毛发开始重新生长，这表明脱发是由哺乳期传播的因素引发的。来自I10−/−母鸡的母乳在体外诱导巨噬细胞分泌促炎细胞因子，无论它们的幼崽是否患上了脱发。饲喂含铁3-6 ppm的饲料可使肥大细胞缺陷仔鼠的脱发窝窝率提高到100%，而肥大细胞缺陷仔鼠的脱发发生率为0%。当喂食含有131ppm铁的饲料时，有脱发的幼崽的血红蛋白和红细胞压积显著低于没有脱发的幼崽(71%；7窝中有5窝)。C-kit的基因或药物抑制导致幼崽肥大细胞枯竭，从而防止了高危幼崽的脱毛。这些研究表明，母体限铁饮食增加了IL-10缺乏的小鼠脱发的发生率，并表明肥大细胞是潜在的效应细胞。进一步的研究表明要进一步探索相关的机制，并确定肥大细胞如何在人类脱发中起作用。
Please cite this paper as:Alopecia in IL‐10‐deficient mouse pups is c‐kit‐dependent and can be triggered by iron deficiency. Experimental Dermatology 2010; 19: 518–526.Abstract:Hair loss (alopecia) can result from a variety of metabolic, endocrine, immunologic, and environmental causes. This investigation was undertaken to determine the mechanisms underlying the sporadic development of alopecia in litters from C57BL/6 interleukin‐10‐deficient (Il10−/−) mice. All pups in affected litters demonstrated alopecia by postnatal days 17–19, with hair loss from their trunks but not from their head, base of tail, or feet. Histopathology revealed distorted hair follicles containing broken hair shafts and prominent dermal infiltrates containing increased numbers of activated mast cells. Hair re‐growth began soon after weaning, suggesting that the alopecia was triggered by factors transmitted during lactation. Milk fromIl10−/−dams induced macrophage secretion of pro‐inflammatory cytokinesin vitroregardless of whether or not their pups developed alopecia. Feeding dams a diet containing 3–6 ppm iron increased the percentage of litters with alopecia to 100% for pups with mast cells, with 0% alopecia in mast cell‐deficient pups. When dams were fed a diet containing 131 ppm iron, significantly lower haemoglobin and hematocrit values were observed in pups from litters with alopecia (71%; 5 of 7 litters) compared to litters without alopecia. Genetic or pharmacologic inhibition of c‐kit that resulted in depletion of mast cells in pups prevented hair loss in at‐risk litters. These studies demonstrate that maternal iron‐restricted diets enhance the incidence of alopecia in IL‐10‐deficient mouse pups and suggest mast cells as potential effector cells. Further studies are indicated to further explore the mechanisms involved and to determine how mast cells may contribute to alopecia in humans.