Institution for Biomedicine, Department of Infectious Disease, University of Gothenburg, Gothenburg, Sweden.
Department of Paediatrics, Institution of Clinical Science, University of Gothenburg, Gothenburg, Sweden.
Br J Dermatol. 2019 Jun;180(6):1481-1488. doi: 10.1111/bjd.17451. Epub 2019 Jan 15.
Insufficient early immune stimulation may predispose to atopic disease. Staphylococcus aureus, a skin and gut colonizer, produces the B-cell mitogen protein A and T-cell-activating superantigens. Early gut colonization by S. aureus strains that possess the superantigens encoded by the enterotoxin gene (egc) cluster and elastin-binding protein is negatively associated with development of atopic eczema.
To investigate (i) whether these findings could be replicated in a second birth cohort, FARMFLORA, and (ii) whether nasal colonization by S. aureus also relates to subsequent atopic eczema development.
Faecal samples and nasal swabs from infants in the FARMFLORA birth cohort (n = 65) were cultured for S. aureus. Individual strains were distinguished by random amplified polymorphic DNA and assessed for adhesin and superantigen gene carriage by polymerase chain reaction. Atopic eczema at 18 months of age was related to nasal and gut S. aureus colonization patterns during the first 2 months of life (well before onset of eczema).
Staphylococcus aureus colonization per se was unrelated to subsequent eczema development. However, gut S. aureus strains from the infants who subsequently developed atopic eczema less frequently carried the ebp gene, encoding elastin-binding protein, and superantigen genes encoded by egc, compared with strains from children who remained healthy. Nasal colonization by S. aureus was less clearly related to subsequent eczema development.
The results precisely replicate our previous observations and may suggest that mucosal colonization by certain S. aureus strains provides immune stimulation that strengthens the epithelial barrier and counteracts the development of atopic eczema.
早期免疫刺激不足可能使机体易患特应性疾病。金黄色葡萄球菌是皮肤和肠道的定植菌，可产生 B 细胞有丝分裂原蛋白 A 和 T 细胞激活超抗原。早期定植于金黄色葡萄球菌的肠道菌株，其携带肠毒素基因（egc）簇和弹性蛋白结合蛋白编码的超抗原，与特应性湿疹的发展呈负相关。
研究（i）这些发现是否可以在第二个出生队列 FARMFLORA 中得到复制，（ii）金黄色葡萄球菌鼻腔定植是否也与随后发生的特应性湿疹有关。
从 FARMFLORA 出生队列的婴儿（n = 65）中采集粪便样本和鼻腔拭子，培养金黄色葡萄球菌。通过随机扩增的多态性 DNA 区分个体菌株，并通过聚合酶链反应评估黏附素和超抗原基因的携带情况。18 个月时的特应性湿疹与生命头 2 个月的鼻腔和肠道金黄色葡萄球菌定植模式有关（在湿疹发病前）。
金黄色葡萄球菌定植本身与随后的湿疹发展无关。然而，与那些未患湿疹的儿童相比，随后发生特应性湿疹的婴儿肠道金黄色葡萄球菌株较少携带编码弹性蛋白结合蛋白的 ebp 基因和 egc 编码的超抗原基因。金黄色葡萄球菌鼻腔定植与随后的湿疹发展关系不明确。
结果精确复制了我们之前的观察结果，可能表明某些金黄色葡萄球菌菌株的黏膜定植提供了免疫刺激，增强了上皮屏障，并抑制了特应性湿疹的发展。
