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Phagocytosis of Aspergillus fumigatus conidia by primary nasal epithelial cells in vitro.
Botterel F., Gross K., Ibrahim-Granet O., Khoufache K., Escabasse V., Coste A., Cordonnier C., Escudier E., Bretagne S.
BMC Microbiology 8 (2008) 97 - http://www.hal.inserm.fr/inserm-00303264
(18564423)
Phagocytosis of Aspergillus fumigatus conidia by primary nasal epithelial cells in vitro.
Françoise Botterel1, Karine Gross1, Oumaïma Ibrahim-Granet2, Khaled Khoufache1, Virginie Escabasse3, 4, André Coste3, 4, Catherine Cordonnier5, Estelle Escudier3, 6, Stéphane Bretagne () 1
1 :  Laboratoire de Parasitologie-Mycologie
Hôpital Henri Mondor – Assistance publique - Hôpitaux de Paris (AP-HP) – Université Paris-Est Créteil Val-de-Marne (UPEC)
Créteil
France
2 :  Aspergillus
Institut Pasteur de Paris
25 rue du Docteur Roux F-75724 Paris cedex 15
France
3 :  Physiopathologie et Thérapeutiques Respiratoires
INSERM : U492 – IFR10
France
4 :  Service d'ORL et de Chirurgie Cervico-Faciale
CHI Créteil
France
5 :  Service d'hématologie clinique
Assistance publique - Hôpitaux de Paris (AP-HP) – Hôpital Henri Mondor – Université Paris-Est Créteil Val-de-Marne (UPEC)
Créteil
France
6 :  Département de Génétique Cytogénétique et Embryologie
Assistance publique - Hôpitaux de Paris (AP-HP) – Hôpital Pitié-Salpêtrière – Université Pierre et Marie Curie (UPMC) - Paris VI
47-83, boulevard de l'Hôpital 75651 PARIS Cedex 13
France
BACKGROUND: Invasive aspergillosis, which is mainly caused by the fungus Aspergillus fumigatus, is an increasing problem in immunocompromised patients. Infection occurs by inhalation of airborne conidia, which are first encountered by airway epithelial cells. Internalization of these conidia into the epithelial cells could serve as a portal of entry for this pathogenic fungus. RESULTS: We used an in vitro model of primary cultures of human nasal epithelial cells (HNEC) at an air-liquid interface. A. fumigatus conidia were compared to Penicillium chrysogenum conidia, a mould that is rarely responsible for invasive disease. Confocal microscopy, transmission electron microscopy, and anti-LAMP1 antibody labeling studies showed that conidia of both species were phagocytosed and trafficked into a late endosomal-lysosomal compartment as early as 4 h post-infection. In double immunolabeling experiments, the mean percentage of A. fumigatus conidia undergoing phagocytosis 4 h post-infection was 21.8 +/- 4.5%. Using combined staining with a fluorescence brightener and propidium iodide, the mean rate of phagocytosis was 18.7 +/- 9.3% and the killing rate 16.7 +/- 7.5% for A. fumigatus after 8 h. The phagocytosis rate did not differ between the two fungal species for a given primary culture. No germination of the conidia was observed until 20 h of observation. CONCLUSION: HNEC can phagocytose fungal conidia but killing of phagocytosed conidia is low, although the spores do not germinate. This phagocytosis does not seem to be specific to A. fumigatus. Other immune cells or mechanisms are required to kill A. fumigatus conidia and to avoid further invasion.
Sciences du Vivant/Biochimie, Biologie Moléculaire
Anglais
1471-2180

Articles dans des revues avec comité de lecture
10.1186/1471-2180-8-97
BMC Microbiology (BMC Microbiol)
Publisher BioMed Central
ISSN 1471-2180 
internationale
2008
18/06/2008
8
97

Aspergillosis – Aspergillus fumigatus – Cell Adhesion – Cells – Cultured – Epithelial Cells – Humans – Nasal Mucosa – Penicillium chrysogenum – Phagocytosis – Spores – Fungal – Virulence
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