id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-001473-aki28lhp	Chen, Qi Xing	Silencing airway epithelial cell-derived hepcidin exacerbates sepsis-induced acute lung injury	2014-08-06		.txt	text/plain	4507	258	44	The knockdown of airway epithelial cell-derived hepcidin aggravated the polymicrobial sepsis-induced lung injury and pulmonary bacterial infection and increased mortality (53.33% in Ad-shHepc1-treated mice versus 12.5% in Ad-shNeg-treated mice, P <0.05). The severe lung injury in the airway epithelial cell-derived hepcidin knockdown mice is at least partially related to the altered intracellular iron level and function of alveolar macrophages. These results demonstrated that in the current study the intratracheal administration of Ad-shHepc1 only silenced the hepcidin gene transcription in AECs, which was in accordance with previous studies that adenovirus-mediated intratracheal gene delivery specifically inhibited targeted gene expression in lung epithelial cells but not in alveolar macrophages and other organs [29, 30] . The current study explored the role of AEC-derived hepcidin in polymicrobial sepsis-induced ALI, which is at least partially related to the altered intracellular iron level and function of alveolar macrophages.	./cache/cord-001473-aki28lhp.txt	./txt/cord-001473-aki28lhp.txt