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Angiogenesis in the lung involves the systemic bronchial vasculature and becomes prominent when chronic inflammation prevails. Mechanisms for neovascularization following pulmonary ischemia include growth factor transit from ischemic parenchyma to upstream bronchial arteries, inflammatory cell migration-recruitment through the perfusing artery, and paracrine effects of lung cells within the left bronchus, the niche where arteriogenesis takes place. We analyzed left lung bronchoalveolar lavage BAL fluid and left bronchus homogenates after left pulmonary artery ligation LPAL in rats, immediately after the onset of ischemia 0 h, 6 h and 24 h later. Additionally, we tested the effectiveness of dexamethasone on decreasing inflammation 0–24 h LPAL and angiogenesis at early 3 d LPAL; bronchial endothelial proliferation and late 14 d LPAL; blood flow stages. After LPAL 6 h, BAL protein, total inflammatory cells, macrophages, and polymorphonuclear cells increased significantly. In parallel, pro-angiogenic CXC chemokines increased in BAL and the left main-stem bronchus CXCL1 or only within the bronchus CXCL2. Dexamethasone treatment reduced total BAL protein, inflammatory cells total and polymorphonuclear cells, and CXCL1 but not CXCL2 in BAL. By contrast, no decrease was seen in either chemokine within the bronchial tissue, in proliferating bronchial endothelial cells, or in systemic perfusion of the left lung. Our results confirm the presence of CXC chemokines within BAL fluid as well as within the left mainstem bronchus. Despite significant reduction in lung injury and inflammation with dexamethasone treatment, chemokine expression within the bronchial tissue as well as angiogenesis were not affected. Our results suggest that early changes within the bronchial niche contribute to subsequent neovascularization during pulmonary ischemia.

Autor: Maria Grazia Perino, Aigul Moldobaeva, John Jenkins, Elizabeth M. Wagner



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