作者: Vishukumar Aimanianda , Jagadeesh Bayry , Silvia Bozza , Olaf Kniemeyer , Katia Perruccio
DOI: 10.1038/NATURE08264
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摘要: The air we breathe is filled with thousands of fungal spores (conidia) per cubic metre, which in certain composting environments can easily exceed 10(9) metre. They originate from more than a hundred species belonging mainly to the genera Cladosporium, Penicillium, Alternaria and Aspergillus. Although these conidia contain many antigens allergens, it not known why airborne microflora do activate host innate immune cells continuously induce detrimental inflammatory responses following their inhalation. Here show that surface layer on dormant masks recognition by system hence prevents response. To explore this, used several members microflora, including human opportunistic pathogen Aspergillus fumigatus, vitro assays dendritic alveolar macrophages vivo murine experiments. In A. this 'rodlet layer' composed hydrophobic RodA protein covalently bound conidial cell wall through glycosylphosphatidylinositol-remnants. extracted fumigatus was immunologically inert did or macrophage maturation activation, failed helper T-cell vivo. removal 'rodlet/hydrophobin either chemically (using hydrofluoric acid), genetically (DeltarodA mutant) biologically (germination) resulted morphotypes inducing activation. All observations rodlet silences moulds.