Lack of matrix metalloproteinase 3 in mouse models of lung injury ameliorates the pulmonary inflammatory response in female but not in male mice
| Autor: | Lynda McCaig, Valeria Puntorieri, Li-Juan Yao, James F. Lewis, Christopher J. Howlett, Cory Yamashita, Ruud A. W. Veldhuizen |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Pulmonary and Respiratory Medicine Lipopolysaccharides Male MMP3 ARDS Pathology medicine.medical_specialty Clinical Biochemistry Acute Lung Injury Inflammation Lung injury Pathogenesis 03 medical and health sciences Mice 0302 clinical medicine Sex Factors Medicine Animals Humans Diffuse alveolar damage Molecular Biology Respiratory Distress Syndrome Lung business.industry Pneumonia respiratory system medicine.disease body regions CXCL1 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Immunology Female Matrix Metalloproteinase 3 Hydrochloric Acid medicine.symptom business |
| Zdroj: | Experimental lung research. 42(7) |
| ISSN: | 1521-0499 |
| Popis: | Background: The acute respiratory distress syndrome (ARDS) is a complex pulmonary disorder in which the local release of cytokines and chemokines appears central to the pathophysiology. Objective: Based on the known role of matrix metalloproteinase-3 (MMP3) in inflammatory processes, the objective was to examine the role of MMP3 in the pathogenesis of ARDS through the modulation of pulmonary inflammation. Materials and Methods: Female and male, wild type (MMP3+/+) and knock out (MMP3−/−) mice were exposed to two, clinically relevant models of ARDS including (i) lipopolysaccharide (LPS)-induced lung injury, and (ii) hydrochloric acid-induced lung injury. Parameters of lung injury and inflammation were assessed through measurements in lung lavage including total protein content, inflammatory cell influx, and concentrations of mediators such as TNF-α, IL-6, G-CSF, CXCL1, CXCL2, and CCL2. Lung histology and compliance were also evaluated in the LPS model of injury. Results: Following intra-tracheal LP... |
| Databáze: | OpenAIRE |
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