id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-018439-4btpqlxd	Kato, Akane	Pathogenesis of COPD (Persistence of Airway Inflammation): Why Does Airway Inflammation Persist After Cessation of Smoking?	2016-07-06		.txt	text/plain	5007	279	43	Initially, cigarette smoke influences the expression of pattern recognition receptors (PRRs) including Toll-like receptors (TLRs), the intracellularly located nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs), retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), and receptors for advanced glycation end products (RAGE) on lung epithelial cells, endothelial cells, and leukocytes in the lung. Global Initiative for Chronic Obstructive Lung Disease 2006 (GOLD 2006) states that "Smoking cessation is the single most effective and cost-effective intervention in most people to reduce the risk of developing COPD and stop its progression (Evidence A)." However, once a patient smokes and develops COPD, the inflammatory changes persist through the innate and adaptive immune systems, which are commonly activated during infection. The hypersecretion of mucus, formation of emphysema, and fibrosis in COPD begin with the inhalation of cigarette smoke, which acts on epithelial cells, macrophages, and T lymphocytes in the airway lumen.	./cache/cord-018439-4btpqlxd.txt	./txt/cord-018439-4btpqlxd.txt