Article Source ~ Clinical Microbiology Review
A. fumigatus interactions with phagocytes. Alveolar macrophages phagocytose inhaled conidia via PRRs. Conidial swelling (within or outside of the macrophage) releases the protective rodlet layer, exposing β(1,3)-glucan for recognition by dectin-1. Dectin-1-β(1,3)-glucan interactions are primarily responsible for the activation of macrophage proinflammatory responses, including conidial killing. Neutrophils attach to hyphae and degranulate, damaging hyphae by oxidative and nonoxidative mechanisms. Neutrophils may also aggregate conidia and prevent germination. Compromised phagocyte function is the primary risk factor for IA. Fungal products (shown in red) may contribute to fungal pathogenicity in these immunocompromised hosts by evading or modulating host defenses.