id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-017470-sjk7a34u	Arlati, Sergio	Pathophysiology of Acute Illness and Injury	2018-06-14		.txt	text/plain	16280	913	34	The endothelium is a key factor for production of remote organ damage as it exerts potent chemo-attracting effects on inflammatory cells, allows for leukocyte trafficking into tissues and organs, and promotes further inflammation by cytokines release. Thus, pneumococcal pneumonia can transform into severe sepsis or septic shock if a generalized inflammatory reaction develops by either cellular (neutrophils, monocytes, macrophages, endothelium) or humoral effectors (complement, contact phase proteins, leukotrienes, cytokines, chemokines) resulting into increased capillary permeability (tissue edema), vasodilation (hypotension), and coagulation activation (ischemic organ damage). However, the severe decrease of innate immune function and the widespread hibernation of nonimmune cell type (cellular hibernation response) [137, 138] make apoptosis a primary mechanism for multiple organ dysfunction and ultimately death. The loss of physiologic anticoagulation in sepsis results from the action of several humoral (IL1-β, TNF-α, and IL6, C-reactive protein) and cellular (vascular endothelial cells, monocytes, macrophages, and platelet) pro-inflammatory mediators.	./cache/cord-017470-sjk7a34u.txt	./txt/cord-017470-sjk7a34u.txt