ReviewAmerican journal of physiology. Lung cellular and molecular physiology2026
The role of myeloid immune cells in lung epithelial repair.
Review in American journal of physiology. Lung cellular and molecular physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The lung epithelium is continuously exposed to injury via pathogens and pollutants, and its capacity for healthy, nonpathological repair is essential to maintain structure and function. In homeostatic repair, type 2 alveolar epithelial (AT2) cells-the stem cells of the alveolar epithelium-differentiate into type 1 alveolar epithelial (AT1) cells in a timed, proportionate process restoring normal epithelial architecture. When dysregulated, this process can result in pathological remodeling, potentially resulting in disease. Myeloid immune cells are among the first responders to lung injury and remain engaged across the full arc of the repair response, yet their contribution to healthy epithelial repair remains underappreciated. In this mini-review, we evaluate current evidence on the role of myeloid immune cells-mononuclear phagocytes and granulocytes-in nonpathological lung epithelial repair. Macrophages promote epithelial proliferation, migration, and barrier restoration through release of soluble mediators including oncostatin M, trefoil factor family, interleukin-1β, and tumor necrosis factor alpha, as well as through extracellular vesicle-mediated communication. Neutrophils contribute through β-catenin signaling, efferocytosis-driven macrophage reprogramming, matrix metalloproteinase-9-dependent remodeling, and direct transfer of microRNA-223 to epithelial cells. Eosinophils, mast cells, and basophils have emerging roles through granule-derived mediators and cross talk with other myeloid cells. Understanding the mechanisms by which myeloid cells promote healthy repair and how dysregulation drives pathological remodeling may uncover therapeutic targets for restoring epithelial function after lung injury.
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