Identification of bacterial biofilm and the Staphylococcus aureus derived protease, staphopain, on the skin surface of patients with atopic dermatitis
Identification of bacterial biofilm and the Staphylococcus aureus derived protease, staphopain, on the skin surface of patients with atopic dermatitis
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DOI：
10.1038/s41598-017-08046-2
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发表时间：
2017-08-18
影响因子：
4.6
通讯作者：
Schmidtchen, Artur
中科院分区：
文献类型：
--
作者：
Sonesson, Andreas;Przybyszewska, Kornelia;Schmidtchen, Artur
特应性皮炎（AD）是一种慢性炎症性皮肤病，其特征是表皮屏障受损，先天性和适应性免疫失调，以及对细菌定植和感染的高度易感性。在本研究中，通过电子显微镜观察AD皮肤表面的细菌生物膜。相应地，金黄色葡萄球菌（S.金黄色葡萄球菌）分离物在体外产生大量的生物膜。S.与使用浮游细胞获得的结果相比，金黄色葡萄球菌生物膜对抗菌肽LL-37的杀伤敏感性较低。共聚焦显微镜分析显示LL-37与S.金黄色葡萄球菌生物膜免疫胶体金染色。AD皮肤金黄色葡萄球菌生物膜检测到S.金黄色葡萄球菌衍生的蛋白酶葡萄球菌蛋白酶邻近细菌。在体外，葡萄球菌蛋白酶B将LL-37降解成较短的肽片段。LL-37对S.金黄色葡萄球菌生物膜的形成，但没有观察到这样的效果的降解产物。本文提供的数据为葡萄球菌中葡萄球菌蛋白的研究提供了新的信息。金黄色葡萄球菌生物膜在体内，并说明生物膜和LL-37之间的复杂的相互作用，在AD患者的皮肤，可能会导致一个不安的宿主防御，这有利于细菌的持久性。
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by an impaired epidermal barrier, dysregulation of innate and adaptive immunity, and a high susceptibility to bacterial colonization and infection. In the present study, bacterial biofilm was visualized by electron microscopy at the surface of AD skin. Correspondingly, Staphylococcus aureus (S. aureus) isolates from lesional skin of patients with AD, produced a substantial amount of biofilm in vitro. S. aureus biofilms showed less susceptibility to killing by the antimicrobial peptide LL-37 when compared with results obtained using planktonic cells. Confocal microscopy analysis showed that LL-37 binds to the S. aureus biofilms. Immuno-gold staining of S. aureus biofilm of AD skin detected the S. aureus derived protease staphopain adjacent to the bacteria. In vitro, staphopain B degraded LL-37 into shorter peptide fragments. Further, LL-37 significantly inhibited S. aureus biofilm formation, but no such effects were observed for the degradation products. The data presented here provide novel information on staphopains present in S. aureus biofilms in vivo, and illustrate the complex interplay between biofilm and LL-37 in skin of AD patients, possibly leading to a disturbed host defense, which facilitates bacterial persistence.