Temporal shifts in post-asthmatic immune responses define lung tumor outcomes via strain-specific monocyte reprogramming [RNA-seq]

We hypothesize that this heterogeneity stems from the temporal dynamics of the inflammatory response and the genetic background of the host. Using ovalbumin (OVA)-induced asthma models, we identify a temporal shift in the immune effector cells driving post-asthmatic tumorigenesis.

During acute airway inflammation, eosinophil infiltration universally accelerates tumor growth across different mouse strains. However, following the resolution of acute inflammation, tumorigenic outcomes during the recovery phase diverge strictly along genetic lines. The prior asthmatic episode leaves a long-lasting epigenetic imprint on bone marrow myeloid progenitors, establishing an innate immune memory that differentially programs monocytes across strains.