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Review
. 2007 Nov;6(11):1953-63.
doi: 10.1128/EC.00274-07. Epub 2007 Sep 21.

Aspergillus fumigatus: principles of pathogenesis and host defense

Tobias M Hohl  1 , Marta Feldmesser
Affiliations
Review

Aspergillus fumigatus: principles of pathogenesis and host defense

Tobias M Hohl et al. Eukaryot Cell. 2007 Nov.
No abstract available

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Figures

FIG. 1.
FIG. 1.
Molecular features of A. fumigatus conidia and hyphae. Schematic representation of resting conidia (top) and hyphae (bottom). The organization of the conidial cell wall is depicted, together with specific conidial and hyphal cell wall and secreted components. Host receptors and products that interact with fungal molecules are listed in blue.
FIG. 2.
FIG. 2.
Classification of A. fumigatus mutants based on phenotypic characteristics that favor fungal growth or clearance in immunocompromised hosts. A. fumigatus hypervirulent (green ovals) and hypovirulent (pink ovals) mutants show phenotypic differences in conidial melanin content, resistance to oxidative assault, germination rates, and hyphal growth. Differences in these phenotypic characteristics, either individually or in aggregate, likely contribute to either fungal tissue invasion or clearance in immunocompromised hosts.
FIG. 3.
FIG. 3.
Stage-specific innate immune responses to A. fumigatus. Inhaled conidia bind soluble receptors, for example, pentraxin-3 and lung surfactant protein D, that enhance inflammatory responses. Conidial swelling can occur in the bronchoalveolar space or within alveolar macrophage phagosomes and results in β-glucan surface exposure, triggering inflammatory and fungicidal responses through the mammalian β-glucan receptor, dectin-1. TLR2- and TLR4-dependent signals contribute to host recognition of germinating conidia and hyphae, as well. Recruited neutrophils cooperate to inactivate conidia and, together with alveolar macrophages, prevent conidial germination in immune-competent hosts. The generation of fungicidal ROIs, for example, superoxide anions (O2·−), is critical to this process. The release of neutrophil granules activates ROI-independent mechanisms to limit fungal growth; these include lactoferrin, a molecule that sequesters iron. In the setting of hyphal tissue invasion, neutrophils attach to fungal cells and degranulate, thus attacking hyphae with ROI-dependent and -independent mechanisms. Dendritic cells and NK cells (not shown) contribute to innate immune defense in specific circumstances, particularly in the setting of defective neutrophil activity (see the text).
See this image and copyright information in PMC

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