Hammond Margaret, Gamal Ahmed, Mukherjee Pranab K, Damiani Giovanni, McCormick Thomas S, Ghannoum Mahmoud A, Nedorost Susan
Department of Dermatology, University Hospitals Cleveland Medical Center/Case Western Reserve University School of Medicine, Cleveland, OH, United States.
Department of Biomedical, Surgical and Dental Sciences University of Milan, Milan, Italy.
Front Microbiol. 2022 Nov 14;13:944365. doi: 10.3389/fmicb.2022.944365. eCollection 2022.
Atopic dermatitis (AD) is associated with cutaneous dysbiosis, barrier defects, and immune dysregulation, but the interplay between these factors needs further study. Early-onset barrier dysfunction may facilitate an innate immune response to commensal organisms and, consequently, the development of allergic sensitization. We aimed to compare the cutaneous microbiome in patients with active dermatitis with and without a history of childhood flexural dermatitis (atopic dermatitis). Next-gen Ion-Torrent deep-sequencing identified AD-associated changes in the skin bacterial microbiome ("bacteriome") and fungal microbiome ("mycobiome") of affected skin in swabs from areas of skin affected by dermatitis. Data were analyzed for diversity, abundance, and inter-kingdom correlations. Microbial interactions were assessed in biofilms using metabolic activity (XTT) assay and scanning electron microscopy (SEM), while host-pathogen interactions were determined in cultured primary keratinocytes exposed to biofilms. Increased richness and abundance of , and were found in atopics. and formed robust mixed-species biofilms (based on XTT and SEM) that were resistant to antifungals/antimicrobials. Furthermore, their biofilm supernatant was capable of influencing keratinocytes biology (pro-inflammatory cytokines and structural proteins), suggesting an additive effect on AD-associated host response. In conclusion, microbial inter-kingdom and host-microbiome interactions may play a critical role in the modulation of atopic dermatitis to a greater extent than in non-atopic adults with allergic contact dermatitis.
特应性皮炎（AD）与皮肤微生物失调、屏障缺陷和免疫调节异常有关，但这些因素之间的相互作用尚需进一步研究。早期发生的屏障功能障碍可能会促进对共生生物的先天性免疫反应，进而导致过敏性致敏的发生。我们旨在比较有和没有儿童期屈侧皮炎（特应性皮炎）病史的活动性皮炎患者的皮肤微生物群。下一代离子激流深度测序确定了来自皮炎受累皮肤区域拭子中受影响皮肤的皮肤细菌微生物群（“细菌组”）和真菌微生物群（“真菌组”）中与AD相关的变化。对数据进行了多样性、丰度和跨界相关性分析。使用代谢活性（XTT）测定法和扫描电子显微镜（SEM）评估生物膜中的微生物相互作用，同时在暴露于生物膜的原代培养角质形成细胞中确定宿主-病原体相互作用。在特应性个体中发现了 、 和 的丰富度和丰度增加。 和 形成了对抗真菌药/抗菌药有抗性的强大混合物种生物膜（基于XTT和SEM）。此外，它们的生物膜上清液能够影响角质形成细胞生物学（促炎细胞因子和结构蛋白），表明对AD相关的宿主反应有累加效应。总之，微生物跨界和宿主-微生物群相互作用在特应性皮炎的调节中可能比在患有过敏性接触性皮炎的非特应性成年人中发挥更关键的作用。
