The lungs are continually exposed to harmful pathogens such as Aspergillus fumigatus, and prompt clearance of such pathogens with limited inflammation is needed to avoid dangerous aspergillosis or collateral damage from the immune response. In Science, Hohl and colleagues demonstrate that myeloid cells in the lungs, such as neutrophils, induce an apoptosis-like process of programmed cell death (PCD) in A. fumigatus conidia. This process is dependent on the generation of reactive oxygen species in neutrophils via the NADPH complex. Accordingly, fungi that overexpress the anti-apoptotic protein AfBIR1 are relatively resistant to neutrophil-induced PCD and demonstrate enhanced virulence. This previously unknown PCD-dependent mechanism for the clearance of conidia represents an effective form of lung immunosurveillance that prevents transition of the fungus to its invasive hyphal form; additionally, it suggests a potential target for the pharmacological treatment of fungal infection.

Science 357, 1037–1041 (2017)