University of Alabama at Birmingham (UAB) researchers have found a novel, previously unreported pathogenic entity that is a fundamental link between chronic inflammation and tissue destruction in the lungs of patients with chronic obstructive pulmonary disease (COPD). COPD is the fourth-leading cause of death in the world. This pathogenic entity -- exosomes from activated polymorphonuclear leukocytes (PMNs) -- caused COPD damage when the small, subcellular particles, collected from purified PMNs, were instilled into the lungs of healthy mice. Remarkably, the UAB researchers also collected exosomes from the lung fluids of human patients with COPD and the lung fluids of neonatal ICU babies with the lung disease bronchopulmonary dysplasia; when those human-derived exosomes were instilled into the lungs of healthy mice, they also caused COPD lung damage. Damage was primarily from PMN-derived exosomes from the human lungs. "This report seems to provide the first evidence of the capability of a defined non-infectious subcellular entity to recapitulate disease phenotype when transferred from human to mouse," said J. Edwin Blalock, PhD, Professor of Pulmonary, allergy and Critical Care Medicine in the UAB Department of Medicine. "I think this could be a very profound discovery. A lot of what we have found here will apply in other tissues, depending on the disease." Other diseases marked by immune cell inflammation and tissue destruction include heart attacks, metastatic cancer and chronic kidney disease. The activated PMN exosomes may also contribute to lung damage in othelung diseases that have excessive PMN-driven inflammation, such as cystic fibrosis. The study is reported in the prestigious journal Cell.
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