De Pessemier Britta, López Celia Díez, Taelman Steff, Verdonck Merel, Chen Yang, Stockman Annelies, Lambert Jo, Van de Wiele Tom, Callewaert Chris
Center for Microbial Ecology and Technology, Ghent University, Ghent, Belgium.
Department of Data Analysis and Mathematical Modelling, Ghent University, Ghent, Belgium; BIOLIZARD, Ghent, Belgium.
J Invest Dermatol. 2025 Mar;145(3):605-617.e14. doi: 10.1016/j.jid.2024.07.020. Epub 2024 Aug 14.
Psoriasis is an immune-mediated inflammatory disorder, where the majority of the patients suffer from psoriasis capitis or scalp psoriasis. Current therapeutics remain ineffective to treat scalp lesions. In this study, we present a whole-metagenome characterization of the scalp microbiome in psoriasis capitis. We investigated how changes in the homeostatic cutaneous microbiome correlate with the condition and identified metagenomic biomarkers (taxonomic, functional, virulence factors, antimicrobial resistance genes) that could partly explain its emergence. Within this study, 83 top and back scalp samples from healthy individuals and 64 lesional and nonlesional scalp samples from subjects with untreated psoriasis capitis were analyzed. Using qPCR targeting the 16S and 18S ribosomal RNA genes, we found a significant decrease in microbial load within scalp regions affected by psoriasis compared with that in their nonlesional counterparts. Metagenomic analysis revealed that psoriatic lesions displayed significant lower Cutibacterium species (including C. modestum, C. namnetense, C. granulosum, C. porci), along with an elevation in Staphylococcus aureus. A heightened relative presence of efflux pump protein-encoding genes was detected, suggesting potential antimicrobial resistance mechanisms. These mechanisms are known to specifically target human antimicrobial peptides (including cathelicidin LL-37), which are frequently encountered within psoriasis lesions. These shifts in microbial community dynamics may contribute to psoriasis disease pathogenesis.
银屑病是一种免疫介导的炎症性疾病,大多数患者患有头皮银屑病或头部银屑病。目前的治疗方法对治疗头皮病变仍然无效。在本研究中,我们展示了头部银屑病患者头皮微生物群的全宏基因组特征。我们研究了稳态皮肤微生物群的变化与病情如何相关,并鉴定了部分可以解释其发生的宏基因组生物标志物(分类学、功能、毒力因子、抗菌抗性基因)。在本研究中,分析了来自健康个体的83份头顶和后头皮样本以及来自未经治疗的头部银屑病患者的64份病变和非病变头皮样本。使用针对16S和18S核糖体RNA基因的定量聚合酶链反应,我们发现与非病变对应部位相比,受银屑病影响的头皮区域微生物负荷显著降低。宏基因组分析显示,银屑病病变部位的棒状杆菌属物种(包括适度棒状杆菌、纳姆内棒状杆菌、颗粒棒状杆菌、猪棒状杆菌)显著减少,同时金黄色葡萄球菌增加。检测到编码外排泵蛋白的基因相对丰度增加,提示潜在的抗菌抗性机制。已知这些机制特异性靶向人类抗菌肽(包括杀菌肽LL-37),而这些抗菌肽在银屑病病变中经常出现。微生物群落动态的这些变化可能有助于银屑病的发病机制。