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Stimulation of the α7 Nicotinic Acetylcholine Receptor Protects Against Sepsis by Inhibiting Toll-like Receptor via Phosphoinositide 3-Kinase Activation
Author(s) -
TaeHoon Kim,
Sojin Kim,
SunMee Lee
Publication year - 2013
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1093/infdis/jit669
Subject(s) - methyllycaconitine , nicotine , tlr4 , pharmacology , medicine , cholinergic , nicotinic agonist , pi3k/akt/mtor pathway , agonist , sepsis , nicotinic acetylcholine receptor , lipopolysaccharide , receptor , immunology , signal transduction , endocrinology , chemistry , biochemistry
The Toll-like receptor (TLR) plays an important role in the induction of the hyperinflammatory response and tissue injury in sepsis. The cholinergic antiinflammatory pathway serves as a link between the parasympathetic and innate immune systems. We examined the antiinflammatory effect of nicotine, a potent α7 nicotinic acetylcholine receptor (α7nAChR) agonist, with regard to TLR expression and signaling during sepsis.

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