Staphylococcus aureus Epicutaneous Exposure Drives Skin Inflammation via IL-36-Mediated T Cell Responses.
Staphylococcus aureus Epicutaneous Exposure Drives Skin Inflammation via IL-36-Mediated T Cell Responses.
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金黄色葡萄球菌的表皮暴露通过IL-36介导的T细胞反应驱动皮肤炎症。
DOI：
10.1016/j.chom.2017.10.006
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发表时间：
2017-11-08
影响因子：
30.3
通讯作者：
Miller LS
中科院分区：
文献类型：
--
作者：
Liu H;Archer NK;Dillen CA;Wang Y;Ashbaugh AG;Ortines RV;Kao T;Lee SK;Cai SS;Miller RJ;Marchitto MC;Zhang E;Riggins DP;Plaut RD;Stibitz S;Geha RS;Miller LS
金黄色葡萄球菌的定植有助于特应性皮炎等疾病的皮肤炎症，但涉及的信号通路尚不清楚。在此，表皮S.金黄色葡萄球菌暴露于小鼠皮肤促进由IL-36而不是IL-1α/β、IL-18或IL-33引发的MyD 88依赖性皮肤炎症。相比之下，皮内S.金黄色葡萄球菌攻击促进由IL-1β而不是IL-36启动的MyD 88依赖性宿主防御，表明不同的IL-1细胞因子根据S.金黄色葡萄球菌皮肤暴露。细菌毒力因子PSMα而不是α-毒素或δ-毒素导致皮肤炎症，其由产生IL-17的γδ和CD 4 + T细胞通过T细胞中的直接IL-36 R信号传导驱动。最后，将表达IL-36 R的T细胞过继转移至IL-36 R缺陷小鼠足以介导S.金黄色引起的皮肤炎症。总之，这项研究确定了一个以前未知的途径，S。金黄色葡萄球菌表皮暴露促进涉及IL-36 R/MyD 88依赖性IL-17 T细胞应答的皮肤炎症。特应性皮炎中金黄色葡萄球菌定植导致皮肤炎症，但其潜在机制尚不清楚。Liu等证明，表皮S。接触金黄色葡萄球菌会导致皮肤炎症，这是由细菌PSMα和宿主IL-36 R/MyD 88诱导的T细胞产生IL-17介导的。
Staphylococcus aureus colonization contributes to skin inflammation in diseases such as atopic dermatitis, but the signaling pathways involved are unclear. Herein, epicutaneous S. aureus exposure to mouse skin promoted MyD88-dependent skin inflammation initiated by IL-36 but not IL-1α/β, IL-18 or IL-33. By contrast, an intradermal S. aureus challenge promoted MyD88-dependent host defense initiated by IL-1β rather than IL-36, suggesting that different IL-1 cytokines trigger MyD88-signaling depending on the anatomical depth of S. aureus cutaneous exposure. The bacterial virulence factor PSMα but not α-toxin or δ-toxin contributed to the skin inflammation, which was driven by IL-17-producing γδ and CD4+ T cells via direct IL-36R-signaling in the T cells. Finally, adoptive transfer of IL-36R-expressing T cells to IL-36R-deficient mice was sufficient for mediating S. aureus-induced skin inflammation. Together, this study defines a previously unknown pathway by which S. aureus epicutaneous exposure promotes skin inflammation involving IL-36R/MyD88-dependent IL-17 T cell responses. Staphylococcus aureus colonization during atopic dermatitis contributes to skin inflammation, but the underlying mechanisms are unclear. Liu et al. demonstrate that epicutaneous S. aureus exposure drives skin inflammation, which is mediated by the bacterial PSMα and host IL-36R/MyD88-induced production of IL-17 by T cells.
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DOI：
10.4049/jimmunol.1301481
发表时间：
2014-06-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Foster AM;Baliwag J;Chen CS;Guzman AM;Stoll SW;Gudjonsson JE;Ward NL;Johnston A
通讯作者：
Johnston A
影响因子：
168.9
作者：
DeLeo, Frank R.;Otto, Michael;Kreiswirth, Barry N.;Chambers, Henry F.
通讯作者：
Chambers, Henry F.
影响因子：
--
作者：
Hersh, Adam L.;Chambers, Henry F.;Gonzales, Ralph
通讯作者：
Gonzales, Ralph
影响因子：
6.4
作者：
Fey PD;Endres JL;Yajjala VK;Widhelm TJ;Boissy RJ;Bose JL;Bayles KW
通讯作者：
Bayles KW
影响因子：
16.6
作者：
Davey MS;Willcox CR;Joyce SP;Ladell K;Kasatskaya SA;McLaren JE;Hunter S;Salim M;Mohammed F;Price DA;Chudakov DM;Willcox BE
通讯作者：
Willcox BE