Macrophage Migration Inhibitory Factor Is a Novel Determinant of Cigarette Smoke–Induced Lung Damage

• Published in: American journal of respiratory cell and molecular biology Vol. 51; no. 1; pp. 94 - 103
• Main Authors: Fallica, Jonathan, Boyer, Laurent, Kim, Bo, Serebreni, Leonid, Varela, Lidenys, Hamdan, Omar, Wang, Lan, Simms, Tiffany, Damarla, Mahendra, Kolb, Todd M., Bucala, Richard, Mitzner, Wayne, Hassoun, Paul M., Damico, Rachel
• Format: Journal Article
• Language: English
• Published: United States American Thoracic Society 01.07.2014
• Subjects: Animals; Apoptosis; Apoptosis - drug effects; Blotting, Western; Deoxyribonucleic acid; Disease; DNA; DNA Damage - drug effects; Endothelial Cells - drug effects; Endothelial Cells - pathology; Gene expression; Homeostasis; Humans; Hypoxia; Immunoenzyme Techniques; Inflammation - etiology; Inflammation - metabolism; Inflammation - pathology; Intramolecular Oxidoreductases - physiology; Kinases; Lung - drug effects; Lung - metabolism; Lung - pathology; Macrophage Migration-Inhibitory Factors - physiology; Methods; Mice; Mice, Inbred C57BL; Mice, Knockout; Original Research; Oxidative Stress; Pulmonary Disease, Chronic Obstructive - etiology; Pulmonary Disease, Chronic Obstructive - metabolism; Pulmonary Disease, Chronic Obstructive - pathology; Pulmonary Emphysema - etiology; Pulmonary Emphysema - metabolism; Pulmonary Emphysema - pathology; Smoke - adverse effects; Studies; Transcription factors; Tumor Suppressor Protein p53 - metabolism; apoptosis; cigarette; macrophage migration inhibitory factor; endothelial; emphysema

Cigarette smoke (CS) is the most common cause of chronic obstructive pulmonary diseases (COPD), including emphysema. CS exposure impacts all cell types within the airways and lung parenchyma, causing alveolar tissue destruction through four mechanisms: (1) oxidative stress; (2) inflammation; (3) pro...