肠道菌群失调促进小鼠白癜风
创作:szx 审核:szx 2019年09月11日
  • 在白癜风小鼠模型中,酪氨酸酶反应性T细胞介导了褪色的发生;
  • 抗生素处理诱导了小鼠肠道T细胞的重新分布,氨苄青霉素(而非新霉素)可加速褪色的发生;
  • 氨苄青霉素引起肠道(而非皮肤)菌群失调,而新霉素增加了皮肤中的Treg丰度;
  • 口服氨苄青霉素改变小鼠的肠道通透性,并加剧炎症因子(M-CSF、IL-1α、IL-23、IFN-γ等)的应答,下调2型细胞因子的水平;
  • 氨苄青霉素与新霉素对小鼠T细胞功能产生不同影响。
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szx
Journal of Investigative Dermatology上发表的一项最新研究,发现特定抗生素处理可加速白癜风小鼠模型的疾病进展,提示肠道菌群及其与T细胞的互作在白癜风的发生发展中起到重要作用。
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Antibiotics drive microbial imbalance and vitiligo development in mice

抗生素驱动小鼠的菌群失调及白癜风发展

10.1016/j.jid.2019.08.435

2019-08-28, Article

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Vitiligo is impacted by environmental triggers. We studied the contribution of the microbiome in FH mice, where depigmentation is mediated by tyrosinase-reactive T cells. Mice received oral antibiotics and were monitored for depigmentation. The microbiome was studied in fecal and skin samples by 16S rRNA analysis. Resulting T-cell distributions were evaluated. In untreated mice, pigment loss did not expand to the pelage, whereas mice in the ampicillin group were about 1/3 depigmented at 30 weeks. Contrary to models of autoimmunity that are less dependent on IFN-γ, ampicillin but not neomycin treatment correlated with accelerated disease and reduced bacteria in fecal pellets. Modified cytokine patterns in tissue and serum suggest a response that transcends the gut. Ampicillin-induced depigmentation was accompanied by gut but not skin dysbiosis, and reduced T cells in both sites. Neomycin induced a redistribution of gut T cells and accumulation of skin Tregs. This treatment spurred a Bacteroides-dominated population of fecal bacteria. Reduced diversity is prominent especially after ampicillin treatment, when the gut is dominated by Pseudomonas species. In line with current concepts relating the microbiome and the immune system, we predict that dietary measures might promote skin health and delay vitiligo onset.

First Authors:
Emilia R Dellacecca,Cormac Cosgrove

Correspondence Authors:
I Caroline Le Poole

All Authors:
Emilia R Dellacecca,Cormac Cosgrove,Zhussipbek Mukhatayev,Suhail Akhtar,Victor H Engelhard,Alfred W Rademaker,Katherine Knight,I Caroline Le Poole

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