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Abstract
BackgroundInvasive 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.ResultsWe 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.ConclusionHNEC 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.
Highlights
Invasive aspergillosis, which is mainly caused by the fungus Aspergillus fumigatus, is an increasing problem in immunocompromised patients
To speed up contact between human nasal epithelial cells (HNEC) and fungal conidia, the HNEC were centrifuged and culture medium containing the conidia was immediately removed from the apical side to restore the air-liquid interface, because immersion rapidly leads to dedifferentiation of HNEC
This was confirmed by transmission electron microscopy (TEM), which showed that A. fumigatus conidia were internalized into vacuoles (Figure 2)
Summary
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. IA is an opportunistic infection resulting from inhalation of conidia released by Aspergillus fumigatus, the main species responsible for this disease [4] Due to their small size (2– 3 μm in diameter), these conidia can reach the alveoli where they are normally phagocytosed and killed by alveolar macrophages through the release of reactive oxidant intermediates [5]. The airways epithelium is frequently damaged by chemotherapy, radiation, viral or bacterial infections in immunocompromised patients at risk of IA [7,8]. This damage could trigger invasion from this site. Rabbit tracheal epithelial cells have been shown to internalize A. fumigatus conidia but this internalization has not been quantified [9,12]
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