蛋白酵素
金黄色葡萄球菌
特应性皮炎
嗜酸性粒细胞
主要碱性蛋白
炎症
渗透(HVAC)
趋化因子
医学
免疫学
生物
细菌
酶
生物化学
哮喘
物理
热力学
遗传学
作者
Sabrina Nolan,Nicholas Orlando,Alex J. Lee,Mary S. Wu,J. Zhang,Christine Youn,Laine Feller,Cristina Pontaza,Dustin Dikeman,Nathachit Limjunyawong,Kaitlin Williams,Yu Wang,Daniela Čiháková,Elizabeth A. Jacobsen,Scott K. Durum,Luis A. Garza,Xinzhong Dong,Nathan K. Archer
标识
DOI:10.1073/pnas.2309243121
摘要
Staphylococcus aureus skin colonization and eosinophil infiltration are associated with many inflammatory skin disorders, including atopic dermatitis, bullous pemphigoid, Netherton’s syndrome, and prurigo nodularis. However, whether there is a relationship between S. aureus and eosinophils and how this interaction influences skin inflammation is largely undefined. We show in a preclinical mouse model that S. aureus epicutaneous exposure induced eosinophil-recruiting chemokines and eosinophil infiltration into the skin. Remarkably, we found that eosinophils had a comparable contribution to the skin inflammation as T cells, in a manner dependent on eosinophil-derived IL-17A and IL-17F production. Importantly, IL-36R signaling induced CCL7-mediated eosinophil recruitment to the inflamed skin. Last, S. aureus proteases induced IL-36α expression in keratinocytes, which promoted infiltration of IL-17-producing eosinophils. Collectively, we uncovered a mechanism for S. aureus proteases to trigger eosinophil-mediated skin inflammation, which has implications in the pathogenesis of inflammatory skin diseases.
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