Fleury Orla M, McAleer Maeve A, Feuillie Cécile, Formosa-Dague Cécile, Sansevere Emily, Bennett Désirée E, Towell Aisling M, McLean W H Irwin, Kezic Sanja, Robinson D Ashley, Fallon Padraic G, Foster Timothy J, Dufrêne Yves F, Irvine Alan D, Geoghegan Joan A
Department of Microbiology, Moyne Institute of Preventive Medicine, School of Genetics and Microbiology, Trinity College Dublin, Dublin, Ireland.
Clinical Medicine, Trinity College Dublin, Dublin, Ireland.
Infect Immun. 2017 May 23;85(6). doi: 10.1128/IAI.00994-16. Print 2017 Jun.
skin infection is a frequent and recurrent problem in children with the common inflammatory skin disease atopic dermatitis (AD). colonizes the skin of the majority of children with AD and exacerbates the disease. The first step during colonization and infection is bacterial adhesion to the cornified envelope of corneocytes in the outer layer, the stratum corneum. Corneocytes from AD skin are structurally different from corneocytes from normal healthy skin. The objective of this study was to identify bacterial proteins that promote the adherence of to AD corneocytes. strains from clonal complexes 1 and 8 were more frequently isolated from infected AD skin than from the nasal cavity of healthy children. AD strains had increased ClfB ligand binding activity compared to normal nasal carriage strains. Adherence of single bacteria to corneocytes from AD patients was studied using atomic force microscopy. Bacteria expressing ClfB recognized ligands distributed over the entire corneocyte surface. The ability of an isogenic ClfB-deficient mutant to adhere to AD corneocytes compared to that of its parent clonal complex 1 clinical strain was greatly reduced. ClfB from clonal complex 1 strains had a slightly higher binding affinity for its ligand than ClfB from strains from other clonal complexes. Our results provide new insights into the first step in the establishment of colonization in AD patients. ClfB is a key adhesion molecule for the interaction of with AD corneocytes and represents a target for intervention.
皮肤感染是患有常见炎症性皮肤病特应性皮炎（AD）的儿童中常见且反复出现的问题。[细菌名称]定植于大多数AD患儿的皮肤并使病情加重。定植和感染过程的第一步是细菌黏附于外层角质形成细胞层即角质层的角质包膜。AD皮肤的角质形成细胞在结构上与正常健康皮肤的角质形成细胞不同。本研究的目的是鉴定促进[细菌名称]黏附于AD角质形成细胞的细菌蛋白。来自克隆复合体1和8的[细菌名称]菌株从感染的AD皮肤中分离出的频率高于从健康儿童鼻腔中分离出的频率。与正常鼻腔携带菌株相比，AD菌株的ClfB配体结合活性增加。使用原子力显微镜研究了单个[细菌名称]细菌对AD患者角质形成细胞的黏附情况。表达ClfB的细菌识别分布在整个角质形成细胞表面的配体。与其亲本克隆复合体1临床菌株相比，同基因ClfB缺陷突变体黏附于AD角质形成细胞的能力大大降低。来自克隆复合体1菌株的ClfB与其配体的结合亲和力略高于来自其他克隆复合体菌株的ClfB。我们的结果为AD患者中[细菌名称]定植建立过程的第一步提供了新的见解。ClfB是[细菌名称]与AD角质形成细胞相互作用的关键黏附分子，是一个干预靶点。
