Local depletion of the recruitment of macrophages reduces acute lung injury in rats

2018 
Acute lung injury(ALI) is a respiratory failure caused by a response of the lung against local or systemic injury. In the early stages C-C chemokine ligand-2(CCL2) is upregulated and classically activated chemokine receptor 2(CCR2+)monocytes/macrophages are recruited to the lung. Monocytes/macrophages infiltration into the alveoli enhances tissue inflammation. Aim: To inhibit the recruitment of CCR2+ monocytes/macrophages into the lung by the administration of CCR2 antagonist or an anti-CCL2 antibody. Methods: Lung injury was induced in Sprague-Dawley rats by intratracheal instillation (it) of HCl (0.1mol/L), followed 2h later by it of LPS of Escherichia coli O55:B5(30μg/g body weight). Control rats were treated with saline. 9h later the corresponding animals were it with CCR2 antagonist(1000ug/ml) or an anti-CCL2 antibody(10ug/ml). Animals were sacrificed at day 3. Leucocytes subsets were measured by flow cytometry in blood, bronchoalveolar lavage (BAL), spleen and bone marrow. One-Way-ANOVA and Bonferroni post-hoc test was applied. P Results: Both treatments,CCR2 antagonist and an anti-CCL2 antibody, reduced lung weight and decreased CD11b+cells (neutrophils and monocytes) in the BAL; proving less inflammatory cell infiltration. No changes in monocytes numbers were observed in bone marrow or spleen. Inflammatory markers expression (IL-1β,IL-6 and TNF-α) was significantly reduced in lung tissue in treated animals. Conclusion: Locally CCR2 or CCL2 blockade reduced infiltrated monocyte/macrophages into the lung, without affecting the systemic production. The reduction of CCR2+monocytes/macrophages was associated with a decrease of inflammation in the lung
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