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These mutant mice appeared normal at birth but failed to gain weight appropriately and died by 4\u2005months of age with severe hypoxemia. Defects in airway branching morphogenesis in association with impaired epithelial cell adhesion and migration, as well as alveolarization defects and persistent macrophage-mediated inflammation were identified. Using an inducible system to delete \u03b21 integrin after completion of airway branching, we showed that alveolarization defects, characterized by disrupted secondary septation, abnormal alveolar epithelial cell differentiation, excessive collagen I and elastin deposition, and hypercellularity of the mesenchyme occurred independently of airway branching defects. By depleting macrophages using liposomal clodronate, we found that alveolarization defects were secondary to persistent alveolar inflammation. \u03b21 integrin-deficient alveolar epithelial cells produced excessive monocyte chemoattractant protein 1 and reactive oxygen species, suggesting a direct role for \u03b21 integrin in regulating alveolar homeostasis. Taken together, these studies define distinct functions of epithelial \u03b21 integrin during both early and late lung development that affect airway branching morphogenesis, epithelial cell differentiation, alveolar septation and regulation of alveolar homeostasis.<\/jats:p>","DOI":"10.1242\/dev.117200","type":"journal-article","created":{"date-parts":[[2014,11,14]],"date-time":"2014-11-14T05:30:47Z","timestamp":1415943047000},"page":"4751-4762","source":"Crossref","is-referenced-by-count":58,"title":["Epithelial \u03b21 integrin is required for lung branching morphogenesis and alveolarization"],"prefix":"10.1242","volume":"141","author":[{"given":"Erin J.","family":"Plosa","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Division of Neonatology, Vanderbilt University Medical Center, Nashville, TN 37232, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa R.","family":"Young","sequence":"additional","affiliation":[{"name":"Department of 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