RvD1 ameliorates LPS-induced acute lung injury via the suppression of neutrophil infiltration by reducing CXCL2 expression and release from resident alveolar macrophages
| Autor: | Zhang Huawei, Qian Wang, Qi-Xing Wu, Shu-Yang Xiang, Shengxing Zheng, Yang Ye, Shengwei Jin, Hong-Xia Mei, Abdullahi Mohamed Ali, Hao-Ran Xu |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Lipopolysaccharides ARDS Lipopolysaccharide Docosahexaenoic Acids Immunology Acute Lung Injury Chemokine CXCL2 Lung injury Formyl peptide receptor 2 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Macrophages Alveolar Immunology and Allergy Medicine Animals Lung Pharmacology business.industry respiratory system medicine.disease Mice Inbred C57BL CXCL2 030104 developmental biology medicine.anatomical_structure chemistry Neutrophil Infiltration 030220 oncology & carcinogenesis Tumor necrosis factor alpha business Infiltration (medical) |
| Zdroj: | International immunopharmacology. 76 |
| ISSN: | 1878-1705 |
| Popis: | Acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) are life-threatening critical syndromes characterized by the infiltration of a large number of inflammatory cells that lead to an excessive inflammatory response. Resolvin D1 (RvD1), an endogenous lipid mediator, is believed to have anti-inflammatory and proresolving effects. In the present study, we examined the impact of RvD1 on the pulmonary inflammatory response, neutrophil influx, and lung damage in a murine model of lipopolysaccharide (LPS)-induced ALI. Treatment with RvD1 protected mice against LPS-induced ALI, and compared to untreated mice, RvD1-treated mice exhibited significantly ameliorated lung pathological changes, decreased tumor necrosis factor-α (TNF-α) concentrations and attenuated neutrophil infiltration. In addition, treatment with RvD1 attenuated LPS-induced neutrophil infiltration via the downregulation of CXCL2 expression on resident alveolar macrophages. Finally, BOC-2, which inhibits the RvD1 receptor lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2), reversed the protective effects of RvD1. These data demonstrate that RvD1 ameliorates LPS-induced ALI via the suppression of neutrophil infiltration by an ALX/FPR2-dependent reduction in CXCL2 expression on resident alveolar macrophages. |
| Databáze: | OpenAIRE |
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