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Absence or inhibition of matrix metalloproteinase-8 decreases ventilator-induced lung injury

التفاصيل البيبلوغرافية
العنوان:	Absence or inhibition of matrix metalloproteinase-8 decreases ventilator-induced lung injury
المؤلفون:	Ana Gutiérrez-Fernández, Guillermo M. Albaiceta, Adrián González-López, Cristina Campestre, Antonio Fueyo, Diego Parra, Francisco Taboada, Emilio García-Prieto, Xose S. Puente, Sandra Cabrera, Aurora Astudillo, Carlos López-Otín
المصدر:	American Journal of Respiratory Cell and Molecular Biology American Journal of Respiratory Cell and Molecular Biology; Vol 43
سنة النشر:	2009
مصطلحات موضوعية:	Pulmonary and Respiratory Medicine, Chemokine, Matrix metalloproteinase inhibitor, medicine.medical_treatment, Ventilator-Induced Lung Injury, Clinical Biochemistry, Inflammation, Lung injury, Matrix metalloproteinase, Matrix Metalloproteinase Inhibitors, 03 medical and health sciences, Mice, 0302 clinical medicine, medicine, Animals, Enzyme Inhibitors, Molecular Biology, Lung, 030304 developmental biology, Mechanical ventilation, Mice, Knockout, 0303 health sciences, Tissue Inhibitor of Metalloproteinase-1, medicine.diagnostic_test, biology, business.industry, Pulmonary Gas Exchange, Cell Biology, respiratory system, Hydrogen-Ion Concentration, 3. Good health, Bronchoalveolar lavage, Matrix Metalloproteinase 8, 030228 respiratory system, Matrix Metalloproteinase 9, Immunology, biology.protein, Breathing, Cytokines, Matrix Metalloproteinase 2, medicine.symptom, business, Biomarkers
الوصف:	Mechanical ventilation is a life-saving therapy that can also damage the lungs. Ventilator-induced lung injury (VILI) promotes inflammation and up-regulates matrix metalloproteinases (MMPs). Among these enzymes, MMP-8 is involved in the onset of inflammation by processing different immune mediators. To clarify the role of MMP-8 in a model of VILI and their relevance as a therapeutic target, we ventilated wild-type and MMP-8-deficient mice with low or high pressures for 2 hours. There were no significant differences after low-pressure ventilation between wild-type and knockout animals. However, lack of MMP-8 results in better gas exchange, decreased lung edema and permeability, and diminished histological injury after high-pressure ventilation. Mmp8(-/-) mice had a different immune response to injurious ventilation, with decreased neutrophilic infiltration, lower levels of IFN-γ and chemokines (LPS-induced CXC chemokine, macrophage inflammatory protein-2), and significant increases in anti-inflammatory cytokines (IL-4, IL-10) in lung tissue and bronchoalveolar lavage fluid. There were no differences in MMP-2, MMP-9, or tissue inhibitor of metalloproteinase-1 between wild-type and knockout mice. These results were confirmed by showing a similar protective effect in wild-type mice treated with a selective MMP-8 inhibitor. We conclude that MMP-8 promotes acute inflammation after ventilation with high pressures, and its short-term inhibition could be a therapeutic goal to limit VILI.
تدمد:	1535-4989
الوصول الحر:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4dc0a4f328f9603ba817482d502aec6dTest https://pubmed.ncbi.nlm.nih.gov/19995943Test
حقوق:	CLOSED
رقم الانضمام:	edsair.doi.dedup.....4dc0a4f328f9603ba817482d502aec6d
قاعدة البيانات:	OpenAIRE

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Ventilator-induced lung injury (VILI) promotes inflammation and up-regulates matrix metalloproteinases (MMPs). Among these enzymes, MMP-8 is involved in the onset of inflammation by processing different immune mediators. To clarify the role of MMP-8 in a model of VILI and their relevance as a therapeutic target, we ventilated wild-type and MMP-8-deficient mice with low or high pressures for 2 hours. There were no significant differences after low-pressure ventilation between wild-type and knockout animals. However, lack of MMP-8 results in better gas exchange, decreased lung edema and permeability, and diminished histological injury after high-pressure ventilation. 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