<i>Aspergillus</i>-Host Immune Interactions

Aspergillus fumigatus is an airborne mold and an opportunistic pathogen whose spores are inhaled and cause disease primarily in immunodeficient patient populations. Its clinical spectrum spans allergic syndromes, chronic pulmonary aspergillosis, and life-threatening invasive aspergillosis, with risk concentrated in patients with hematologic malignancy, transplant recipients, individuals receiving corticosteroids or other immunomodulators, and people with structural lung disease. Host protection relies on coordinated mucosal barriers, phagocyte-driven clearance, and finely tuned inflammatory signaling; failure at any step can enable tissue invasion or persistent infection, while excessive inflammation can itself drive pathology. Major challenges in the field include diagnostics, rising antifungal resistance, and an incomplete understanding of which immune pathways confer protection versus immunopathology.This Research Topic aims to provide insight into the dynamic interactions between A. fumigatus and host immune responses across time—spanning immediate recognition to longer-term immune adaptation and memory-like features. A central focus will be the contribution of humoral pattern recognition molecules, as well as how evolving mechanistic insights have shaped contemporary research directions and clinical management. In addition, this collection highlights immunometabolic responses that shape antifungal immunity in the lung and systemically, including how metabolic reprogramming (glycolysis vs oxidative phosphorylation, mitochondrial ROS, lipid metabolism, and iron handling) tunes phagocyte effector functions, cytokine programs, and immunopathology during aspergillosis. By integrating immunology, fungal biology, and translational perspectives, this collection will offer a foundation for future studies that advance control, prevention, and treatment of Aspergillus-related diseases.We welcome articles that investigate but are not limited to the following areas:• Pattern-recognition pathways that drive opsonization, complement activation, and fungal containment• How humoral recognition systems integrate with cellular PRRs to shape antifungal immunity• Early lung events after conidial inhalation: epithelial sensing, barrier responses, mucociliary clearance, and local cytokine/chemokine programs• Phagocyte-mediated control of conidia and hyphae, including neutrophil extracellular traps (NETs), oxidative vs non-oxidative killing, and phagolysosomal mechanisms• Immunometabolic regulation of antifungal defense, including PRR-linked metabolic rewiring in macrophages/neutrophils, mitochondrial function and ROS, lipid mediator biosynthesis, amino acid utilization, and iron/heme sequestration that shape fungal restriction versus immunopathology• Fungal determinants of immune evasion and persistence (cell wall masking/remodeling, melanin, secreted proteases/toxins, stress-response pathways)• Time-resolved immune trajectories from exposure to disease: protective responses, tolerance, trained immunity, and susceptibility to relapse or reinfection• Immune correlates that distinguish colonization, allergy, chronic infection, and invasive disease across patient populations• Biomarkers and immune signatures for risk prediction, diagnosis support, prognosis, and therapy monitoring• Effects of immunosuppression and immunomodulation (corticosteroids, biologics, chemotherapy, transplant regimens) on antifungal defense and inflammatory damage• Multi-omics and systems immunology maps of host–pathogen interactions that identify actionable pathways and targets• Strategies to improve outcomes through host-directed approaches, immunotherapies, and optimized integration with antifungal treatment and stewardship Topic editors: Margherita Bertuzzi, Rita Silva-Gomes, Samuel Gonçalves Source: https://www.frontiersin.org/research-topics/81010/aspergillus-host-immune-interactions