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Peer-reviewedCC BY 4.0Frontiers in Immunology

Airway epithelial cell–lung macrophage crosstalk in type 2-high and low asthma endotypes: mechanisms and therapeutic strategies

  • Yinuo Wang1
  • Yuxuan Sun2
  • Suning Mu1
  • Yan Wang1
  • Chaofan Guo1
  • Youpeng Wang3
  1. 1Faculty of Clinical Medical College, Heilongjiang University of Chinese Medicine
  2. 2Institute of Basic Theory of Chinese Medicine, China Academy of Chinese Medical Sciences
  3. 3Department of Pediatrics, The Second Affiliated Hospital of Heilongjiang University of Chinese Medicine
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Abstract

Asthma is a heterogeneous chronic airway disease. Asthma endotypes are mainly classified as type 2-high and type 2-low, based on immunological and molecular mechanisms, providing a more comprehensive framework for understanding the underlying pathological processes. Airway epithelial cells (AECs) and lung macrophages contribute to airway homeostasis and asthmatic inflammation through communication that can support either tissue protection or disease-associated responses. This narrative review integrates their physiological and pathological functions, focusing on AEC-to-macrophage and macrophage-to-AEC signaling within broader multicellular networks across different asthma endotypes. Direct functional evidence for intercellular communication from associations and indirect mechanisms is distinguished and graded. Therapeutic strategies targeting AECs, lung macrophages, and their crosstalk, including both clinically validated and preclinical approaches, are also discussed. The AEC–macrophage axis exhibits context-dependent signaling that may amplify inflammation or support protective regulation, providing a basis for evaluating potential therapeutic interventions.

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Cite

BibTeXRIS
BibTeX
@article{wang2026airway,
  title = {{Airway epithelial cell–lung macrophage crosstalk in type 2-high and low asthma endotypes: mechanisms and therapeutic strategies}},
  author = {Yinuo Wang and Yuxuan Sun and Suning Mu and Yan Wang and Chaofan Guo and Youpeng Wang},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1985258},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1985258/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Airway epithelial cell–lung macrophage crosstalk in type 2-high and low asthma endotypes: mechanisms and therapeutic strategies
AU  - Yinuo Wang
AU  - Yuxuan Sun
AU  - Suning Mu
AU  - Yan Wang
AU  - Chaofan Guo
AU  - Youpeng Wang
PY  - 2026
DA  - 2026/10/22
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1985258
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1985258/full
AB  - Asthma is a heterogeneous chronic airway disease. Asthma endotypes are mainly classified as type 2-high and type 2-low, based on immunological and molecular mechanisms, providing a more comprehensive framework for understanding the underlying pathological processes. Airway epithelial cells (AECs) and lung macrophages contribute to airway homeostasis and asthmatic inflammation through communication that can support either tissue protection or disease-associated responses. This narrative review integrates their physiological and pathological functions, focusing on AEC-to-macrophage and macrophage-to-AEC signaling within broader multicellular networks across different asthma endotypes. Direct functional evidence for intercellular communication from associations and indirect mechanisms is distinguished and graded. Therapeutic strategies targeting AECs, lung macrophages, and their crosstalk, including both clinically validated and preclinical approaches, are also discussed. The AEC–macrophage axis exhibits context-dependent signaling that may amplify inflammation or support protective regulation, providing a basis for evaluating potential therapeutic interventions.
SN  - 1664-3224
ER  -