Department of Dermatology, Drexel University College of Medicine, Philadelphia, Pennsylvania.
Surgical Infections Research and Bacterial Pathogenesis Program, Drexel University College of Medicine, Philadelphia, Pennsylvania.
JAMA Dermatol. 2014 Mar;150(3):260-5. doi: 10.1001/jamadermatol.2013.8627.
Atopic dermatitis (AD) is thought to be a double-hit phenomenon with an unknown environmental component and a genetic abnormality likely centered on the filaggrin gene. Biologically, the presence of Staphylococcus aureus in AD was reported more than 2 decades ago, but the relationship to AD has been elusive.
To explore the bacteria that produce the biofilms in the lesions of AD and the response of the innate immune system to these biofilm occlusions of the sweat ducts by specifically evaluating Toll-like receptor 2.
DESIGN, SETTING, AND PARTICIPANTS: University hospital dermatologic clinic study involving the environmental component related to the characterization, correlation, and impact of staphylococci and their biofilms in AD. We processed routine skin swabs from lesional and nonlesional skin from 40 patients with AD and performed scrapings and biopsies. We also obtained 20 samples from controls (10 inflamed skin samples and 10 normal skin samples).
Gram staining, bright-field microscopy, hematoxylin and eosin, periodic acid-Schiff, Congo red, and light microscopy.
Association of staphylococcal biofilms with AD pathogenesis.
All AD-affected samples contained multidrug-resistant staphylococci, with S aureus (42.0%) and Staphylococcus epidermidis (20.0%) as the predominant species. All isolates were positive for extracellular polysaccharide and biofilm (85.0% strong biofilm producers and 15.0% moderately to weakly positive). Polymerase chain reaction revealed the biofilm-mediating icaD (93.0%) and aap (12.5%) genes in the isolates (some contained both). We also examined tissues for microbial identification, extracellular biomass formation, biofilm formation, and staphylococcal biofilm in skin tissues. Occlusion of sweat ducts with periodic acid-Schiff-positive and Congo red-positive material was noted on microscopic tissue examination. Toll-like receptor 2 was shown to be activated in AD lesional skin (immediately proximal to the sweat ducts), which likely led to the initiation of proteinase-activated receptor 2-mediated pruritus and MyD88-mediated spongiosis.
Biofilm formation by AD-associated staphylococci almost certainly plays a major role in the occlusion of sweat ducts and leads to inflammation and pruritus. We believe the environmental hit in AD relates to staphylococci and their biofilms, which occlude sweat ducts.
特应性皮炎（AD）被认为是一种双重打击现象，其环境因素未知，遗传异常可能集中在丝聚合蛋白基因上。从生物学角度来看，金黄色葡萄球菌存在于 AD 中已有 20 多年，但与 AD 的关系仍不清楚。
通过专门评估 Toll 样受体 2，探讨 AD 病变中产生生物膜的细菌以及先天免疫系统对这些汗腺生物膜阻塞的反应。
设计、地点和参与者：这是一项大学医院皮肤科诊所研究，涉及与金黄色葡萄球菌及其生物膜的特征、相关性和影响有关的环境因素。我们处理了 40 例 AD 患者皮损和非皮损皮肤的常规皮肤拭子，并进行了刮擦和活检。我们还从 20 名对照者（10 名炎症皮肤样本和 10 名正常皮肤样本）中获得了样本。
革兰氏染色、明场显微镜、苏木精和伊红、过碘酸希夫、刚果红和光镜。
金黄色葡萄球菌生物膜与 AD 发病机制的关联。
所有受 AD 影响的样本均含有多药耐药性金黄色葡萄球菌，其中金黄色葡萄球菌（42.0%）和表皮葡萄球菌（20.0%）为主要菌种。所有分离株均为胞外多糖和生物膜阳性（85.0%强生物膜产生菌和 15.0%中度至弱阳性）。聚合酶链反应显示分离株中存在生物膜介导的 icaD（93.0%）和 aap（12.5%）基因（有些包含两者）。我们还检查了组织中的微生物鉴定、胞外生物量形成、生物膜形成和皮肤组织中的金黄色葡萄球菌生物膜。组织镜检显示，周期性酸-Schiff 阳性和刚果红阳性物质阻塞了汗腺。Toll 样受体 2 在 AD 病变皮肤（紧邻汗腺）中被激活，这可能导致蛋白水解酶激活受体 2 介导的瘙痒和 MyD88 介导的海绵形成的发生。
AD 相关金黄色葡萄球菌的生物膜形成几乎肯定在汗腺阻塞中起主要作用，并导致炎症和瘙痒。我们认为 AD 中的环境因素与金黄色葡萄球菌及其生物膜有关，这些生物膜阻塞了汗腺。
