Temporal shifts in post-asthmatic immune responses define tumor outcomes via strain-specific monocyte reprogramming
Abstract
Epidemiological evidence linking asthma to lung cancer risk remains contradictory, presenting asthma as either a risk factor or a protective condition. We hypothesize that this heterogeneity stems from the temporal dynamics of inflammatory response and host genetic background. Using ovalbumin (OVA)-induced asthma models, we identify a temporal shift in immune effectors driving post-asthmatic tumorigenesis. During acute airway inflammation, eosinophil infiltration accelerates tumor growth across mouse strains. Following resolution, however, tumorigenic outcomes in recovery diverge along genetic lines. Prior asthma reshapes chromatin landscapes of bone marrow myeloid progenitors, establishing innate immune memory that differentially programs monocytes across strains. In C57BL/6 mice, trained monocytes adopt oxidative phosphorylation (OXPHOS), acquiring a suppressive, tissue-remodeling phenotype that promotes tumor progression. Conversely, BALB/c-trained monocytes utilize glycolysis to maintain a pro-phagocytic state, enabling tumor clearance. These findings delineate a biphasic mechanism wherein temporal shifts in post-asthmatic immune responses define tumor outcomes via strain-specific monocyte metabolic reprogramming.
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BibTeX
@article{wang2026temporal,
title = {{Temporal shifts in post-asthmatic immune responses define tumor outcomes via strain-specific monocyte reprogramming}},
author = {Xiunan Wang and Chuanfang Chen and Yantong Wan and Buyun Dang and Xinnan Liu and Qingxiang Gao and Jia Zhang and Shih-Chin Cheng},
journal = {Cell Reports},
year = {2026},
month = nov,
doi = {10.1016/j.celrep.2026.118263},
url = {https://linkinghub.elsevier.com/retrieve/pii/S2211124726013422},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Temporal shifts in post-asthmatic immune responses define tumor outcomes via strain-specific monocyte reprogramming
AU - Xiunan Wang
AU - Chuanfang Chen
AU - Yantong Wan
AU - Buyun Dang
AU - Xinnan Liu
AU - Qingxiang Gao
AU - Jia Zhang
AU - Shih-Chin Cheng
PY - 2026
DA - 2026/11/01
JO - Cell Reports
DO - 10.1016/j.celrep.2026.118263
UR - https://linkinghub.elsevier.com/retrieve/pii/S2211124726013422
AB - Epidemiological evidence linking asthma to lung cancer risk remains contradictory, presenting asthma as either a risk factor or a protective condition. We hypothesize that this heterogeneity stems from the temporal dynamics of inflammatory response and host genetic background. Using ovalbumin (OVA)-induced asthma models, we identify a temporal shift in immune effectors driving post-asthmatic tumorigenesis. During acute airway inflammation, eosinophil infiltration accelerates tumor growth across mouse strains. Following resolution, however, tumorigenic outcomes in recovery diverge along genetic lines. Prior asthma reshapes chromatin landscapes of bone marrow myeloid progenitors, establishing innate immune memory that differentially programs monocytes across strains. In C57BL/6 mice, trained monocytes adopt oxidative phosphorylation (OXPHOS), acquiring a suppressive, tissue-remodeling phenotype that promotes tumor progression. Conversely, BALB/c-trained monocytes utilize glycolysis to maintain a pro-phagocytic state, enabling tumor clearance. These findings delineate a biphasic mechanism wherein temporal shifts in post-asthmatic immune responses define tumor outcomes via strain-specific monocyte metabolic reprogramming.
SN - 2211-1247
ER -