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Significance Chronic obstructive pulmonary disease has generally been considered a non-Th2-type lung disease, in contrast to allergic asthma. We identified unexpected roles for basophils, Th2 cytokine IL-4, and interstitial macrophages in triggering emphysema formation in spite of the fact that basophils account for less than 1% of cellular infiltrates in the lung. Our observations in a series of genetically engineered mice illustrated that basophil-derived IL-4 acts on lung-infiltrating monocytes to promote their differentiation into interstitial macrophages that in turn produce a pathogenic enzyme, matrix metalloproteinase-12 (MMP-12), resulting in the destruction of alveolar walls and leading to emphysema. Thus, the present study has identified a previously unappreciated role for the basophil-derived IL-4/monocyte–derived interstitial macrophage/MMP-12 axis at the initiation phase of emphysema development in mice.

Basophils trigger emphysema development in a murine model of COPD through IL-4–mediated generation of MMP-12–producing macrophages