Aspergillus fumigatus Cell Wall Promotes Apical Airway Epithelial Recruitment of Human Neutrophils

被引:16
|
作者
Feldman, Michael B. [1 ,2 ]
Dutko, Richard A. [3 ]
Wood, Michael A. [4 ]
Ward, Rebecca A. [3 ]
Leung, Hui Min [5 ,6 ]
Snow, Ryan F. [4 ]
De La Flor, Denis J. [4 ]
Yonker, Lael M. [4 ,8 ,9 ]
Reedy, Jennifer L. [3 ,6 ]
Tearney, Guillermo J. [5 ,6 ,7 ]
Mou, Hongmei [4 ,8 ,9 ]
Hurley, Bryan P. [4 ]
Vyas, Jatin M. [2 ,3 ,6 ]
机构
[1] Massachusetts Gen Hosp, Div Pulm & Crit Care Med, Boston, MA 02114 USA
[2] Harvard Med Sch, Dept Med, Boston, MA 02115 USA
[3] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA
[4] Massachusetts Gen Hosp, Dept Pediat, Mucosal Immunol & Biol Res Ctr, Boston, MA 02114 USA
[5] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA
[6] Harvard Med Sch, Boston, MA 02115 USA
[7] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA
[8] Massachusetts Gen Hosp Children, Div Pediat Pulm Med, Boston, MA USA
[9] Harvard Med Sch, Dept Pediat, Boston, MA 02115 USA
基金
美国国家卫生研究院;
关键词
Aspergillus fumigatus; epithelial cells; host-pathogen interactions; neutrophils; respiratory pathogens; HEPOXILIN A(3); PHOSPHOLIPASE A(2); PHAGOCYTOSIS; MIGRATION; CONIDIA; MELANIN; GENE; TRANSMIGRATION; IDENTIFICATION; BIOSYNTHESIS;
D O I
10.1128/IAI.00813-19
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Aspergillus fumigatus is a ubiquitous fungal pathogen capable of causing multiple pulmonary diseases, including invasive aspergillosis, chronic necrotizing aspergillosis, fungal colonization, and allergic bronchopulmonary aspergillosis. Intact mucociliary barrier function and early airway neutrophil responses are critical for clearing fungal conidia from the host airways prior to establishing disease. Following inhalation, Aspergillus conidia deposit in the small airways, where they are likely to make their initial host encounter with epithelial cells. Challenges in airway infection models have limited the ability to explore early steps in the interactions between A. fumigatus and the human airway epithelium. Here, we use inverted air-liquid interface cultures to demonstrate that the human airway epithelium responds to apical stimulation by A. fumigatus to promote the transepithelial migration of neutrophils from the basolateral membrane surface to the apical airway surface. Promoting epithelial transmigration with Aspergillus required prolonged exposure with live resting conidia. Swollen conidia did not expedite epithelial transmigration. Using A. fumigatus strains containing deletions of genes for cell wall components, we identified that deletion of the hydrophobic rodlet layer or dihydroxynaphthalene-melanin in the conidial cell wall amplified the epithelial transmigration of neutrophils, using primary human airway epithelium. Ultimately, we show that an as-yet-unidentified nonsecreted cell wall protein is required to promote the early epithelial transmigration of human neutrophils into the airspace in response to A. fumigatus. Together, these data provide critical insight into the initial epithelial host response to Aspergillus.
引用
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页数:16
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