皮肤微生物群的分泌物调节皮肤对抗Borrelia burgdorferi s.s.s.的天生的免疫力
F Baquer1,2, B Jaulhac3,4,5, C Barthel3
1Institut de Bactériologie, Fédération de Médecine Translationnelle de Strasbourg, University of Strasbourg, UR7290, ITI InnoVec, 3 Rue Koeberlé, 67000, Strasbourg, France. baquer@unistra.fr.
Scientific reports
|September 29, 2023
概括
皮肤微生物群通过调节居民皮肤细胞对Borrelia burgdorferi的反应来影响莱姆病. 结合性细菌主要是质细胞和纤维细胞,在感染过程中产生更快的先天免疫反应.
科学领域:
- 皮肤病学 皮肤病学
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 皮肤是莱姆氏病宿主,细菌和的关键交互点.
- 居住的皮肤细胞 (角质细胞,纤维细胞) 和皮肤微生物群在免疫和炎症中发挥作用.
- 了解这些相互作用对于载体传播疾病研究至关重要.
研究的目的:
- 为了研究人体皮肤细胞和Borrelia burgdorferi之间的体外相互作用.
- 确定开始性皮肤细菌对这种相互作用的影响.
- 阐明居住性皮肤细胞和皮肤微生物组在波雷利亚诱导的炎症中的作用.
主要方法:
- 在人体初级角质细胞和纤维细胞的体外分析.
- 与Borrelia burgdorferi sensu stricto共同培养N40.与Borrelia burgdorferi stricto共同培养N40.与Borrelia burgdorferi stricto sensu stricto共同培养N40.与Borrelia burgdorferi stricto sensu stricto共同培养N40.与Borrelia burgdorferi stricto sensu stricto N40.与Borrelia burgdorferi stricto sensu stricto N40.与Borrelia burgdorferi stricto sensu stricto N40.与Borrelia burgdorferi stricto sensu stricto
- 暴露于来自共生细菌 (Staphylococcus epidermidis,Corynebacterium striatum,Cutibacterium acnes) 的超水生物.
- 对炎症标志物表达的测量 (IL-8,CXCL1,MCP-1,SOD-2,hBD-2). 这是一个很好的方法.
主要成果:
- 复合性细菌超级生物在纤维细胞中增加了IL-8,CXCL1,MCP-1和SOD-2的表达.
- 复合性细菌的超级生物增加了IL-8,CXCL1,MCP-1和hBD-2表达在不分化的角质细胞中.
- 复合性细菌抑制了IL-8,CXCL1和MCP-1在分化的角质细胞中的表达.
- 在所有测试的细胞类型中,Borrelia burgdorferi诱导炎症.
结论:
- 皮肤微生物组显著调节住宿性皮肤细胞对Borrelia burgdorferi的炎症反应.
- 综合性细菌似乎在Borrelia感染时在皮肤细胞中促进了快速的先天免疫反应.
- 居住性皮肤细胞和皮肤微生物群是莱姆病发病的早期发生的重要因素.
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