Myeloid Cell States in Influenza-Associated Pulmonary Aspergillosis are Shaped by Iron Overload and Metabolic Reprogramming

IAPA is a severe complication of influenza ICU-admitted patients, but the host mechanisms that drive susceptibility remain incompletely understood.

To address this, we profiled CD11b+ monocyte/macrophage-enriched lung cells from naïve mice, IAV-only mice, A. fumigatus (CEA10)-only mice, and IAV+A. fumigatus (Coinfection) mice. This dataset provides a high-resolution view of how prior influenza infection reshapes innate immune cell states during secondary A. fumigatus infection. These data establish a resource for investigating innate immune dysregulation in IAPA and offer new insight into how influenza-driven remodeling of the lung myeloid compartment impairs monocyte and macrophage responses to secondary fungal challenge.