本期封面所示為煙曲霉分生孢子的一幅掃描電子顯微鏡照片（由S. Guadagnini,、 J. M. Panaud 和A. Beauvais提供）,，煙曲霉是這項(xiàng)研究中所使用的人類病原體之一。
我們每天都會(huì)吸入數(shù)以千計(jì)的微小真菌孢子（分生孢子）,，它們來自很多不同的真菌菌種,。然而，雖然這些孢子內(nèi)含抗原和過敏原,，但它們的吸入并不會(huì)連續(xù)激發(fā)我們的先天免疫細(xì)胞或引起炎癥反應(yīng),。
一系列免疫學(xué)、生物醫(yī)學(xué)和遺傳學(xué)實(shí)驗(yàn)說明了原因是什么：這些孢子的免疫識(shí)別被覆蓋分生孢子表面的小棒蛋白所構(gòu)成的一個(gè)憎水層阻止了,。如果將這個(gè)憎水層去掉,，孢子就會(huì)激發(fā)免疫系統(tǒng)。具備這一防衛(wèi)層的一個(gè)致病性孢子也許會(huì)一直處于休眠狀態(tài),，躲開宿主防衛(wèi)系統(tǒng),，直到條件合適時(shí)才萌發(fā)。從治療角度來講,，小棒蛋白的這種魯棒性也許可被利用來生成納米顆粒，后者含有嵌入的分子,，這些分子以身體內(nèi)某一特定位置為目標(biāo),，或經(jīng)過了優(yōu)化處理，可以持續(xù)向體內(nèi)輸送,。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 460, 1117-1121 (27 August 2009) | doi:10.1038/nature08264
Surface hydrophobin prevents immune recognition of airborne fungal spores
Vishukumar Aimanianda1,8, Jagadeesh Bayry2,3,4,8, Silvia Bozza5, Olaf Kniemeyer7, Katia Perruccio6, Sri Ramulu Elluru2,3,4, Cécile Clavaud1, Sophie Paris1, Axel A. Brakhage7, Srini V. Kaveri2,3,4, Luigina Romani5 & Jean-Paul Latgé1
1 Unité des Aspergillus, Institut Pasteur, Paris F-75015, France
2 INSERM, U 872,
3 Centre de Recherche des Cordeliers, Université Pierre et Marie Curie–Paris 6, UMR S 872,
4 Université Paris Descartes, UMR S 872, Paris F-75006, France
5 Department of Experimental Medicine and Biochemical Sciences,
6 Clinical Immunology, Department of Clinical and Experimental Medicine, University of Perugia, Perugia 06122, Italy
7 Department of Molecular and Applied Microbiology, Leibniz-Institute for Natural Product Research and Infection Biology (HKI) and Friedrich Schiller University, 07745 Jena, Germany
8 These authors contributed equally to this work.
The air we breathe is filled with thousands of fungal spores (conidia) per cubic metre, which in certain composting environments can easily exceed 109 per cubic metre. They originate from more than a hundred fungal species belonging mainly to the genera Cladosporium, Penicillium, Alternaria and Aspergillus 1, 2, 3, 4. Although these conidia contain many antigens and allergens5, 6, 7, it is not known why airborne fungal microflora do not activate the host innate immune cells continuously and do not induce detrimental inflammatory responses following their inhalation. Here we show that the surface layer on the dormant conidia masks their recognition by the immune system and hence prevents immune response. To explore this, we used several fungal members of the airborne microflora, including the human opportunistic fungal pathogen Aspergillus fumigatus, in in vitro assays with dendritic cells and alveolar macrophages and in in vivo murine experiments. In A. fumigatus, this surface 'rodlet layer' is composed of hydrophobic RodA protein covalently bound to the conidial cell wall through glycosylphosphatidylinositol-remnants. RodA extracted from conidia of A. fumigatus was immunologically inert and did not induce dendritic cell or alveolar macrophage maturation and activation, and failed to activate helper T-cell immune responses in vivo. The removal of this surface 'rodlet/hydrophobin layer' either chemically (using hydrofluoric acid), genetically (rodA mutant) or biologically (germination) resulted in conidial morphotypes inducing immune activation. All these observations show that the hydrophobic rodlet layer on the conidial cell surface immunologically silences airborne moulds.
