id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-002591-kt25ip40	Ponce-Gallegos, Marco Antonio	Th17 profile in COPD exacerbations	2017-06-22		.txt	text/plain	4753	257	45	5 Cell death produced releases damage-associated molecular patterns (DAMPs) such as heat shock proteins, S100 protein and high mobility group box 1 (HMGB1), 14 which are recognized by extracellular receptors present in neutrophils, macrophages and dendritic cells (DCs; such as Toll-like receptors [TLRs], for example) [15] [16] [17] and trigger an intracellular signaling cascade led by the transcription factors Myd88 and NF-κB that culminate in the release of proinflammatory cytokines, such as IL-1β and IL-18 (a multiprotein complex responsible for activating caspase 1 and releasing mature forms of various cytokines), 18 which, together with other cytokines (TNF-α, CXCL8, IL-6, among others), are responsible for the recruitment of leukocytes to the inflammation zone. 39 An important factor associated with the predisposition of COPD patients to present exacerbations is the metaplasia of squamous epithelial cells that appears as a consequence of the damage generated to the airway epithelium by the chemical compounds of the cigarette.	./cache/cord-002591-kt25ip40.txt	./txt/cord-002591-kt25ip40.txt