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Acute ethanol exposure inhibits toll...

Goral, Joanna.

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Acute ethanol exposure inhibits toll-like receptor-mediated inflammatory responses of murine macrophages.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Acute ethanol exposure inhibits toll-like receptor-mediated inflammatory responses of murine macrophages./
Author:	Goral, Joanna.
Description:	156 p.
Notes:	Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2497.
Contained By:	Dissertation Abstracts International66-05B.
Subject:	Health Sciences, Immunology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3174241
ISBN:	0542114658

Acute ethanol exposure inhibits toll-like receptor-mediated inflammatory responses of murine macrophages.
Goral, Joanna.

Acute ethanol exposure inhibits toll-like receptor-mediated inflammatory responses of murine macrophages. - 156 p.

Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2497.

Thesis (Ph.D.)--Loyola University Chicago, 2005.

Ethanol is known to increase susceptibility to infections, in part, by suppressing macrophage function. Through toll-like receptors (TLRs), macrophages recognize pathogens and initiate inflammatory responses. In this study, the effect of acute ethanol exposure on murine macrophage activation mediated via TLR2, TLR4 and TLR9 was investigated. Specifically, the study focused on the pro-inflammatory cytokines IL-6 and TNFalpha and activation of p38 and ERK1/2 mitogen-activated protein kinases (MAPKs) after a single in vivo exposure to physiologically relevant level of ethanol followed by ex vivo stimulation with specific TLR ligands. Acute ethanol treatment inhibited IL-6 and TNFalpha synthesis 3 and 24 hours after administration and impaired p38 and ERK1/2 activation induced by TLR2, TLR4, and TLR9 ligands. We also addressed the question of whether ethanol treatment modified activities of serine/threonine-specific, tyrosine-specific phosphatases, and MAPK phosphatase-1. Inhibitors of three families of protein phosphatases did not restore ethanol-impaired pro-inflammatory cytokines production nor p38 and ERK1/2 activation. However, inhibitors of ser/thr protein phosphatase-type I and -2A (PP1, PP2A) significantly increased IL-6 and TNFalpha levels, and prolonged activation of p38 and ERK1/2 when triggered by TLR4 and TLR9 ligands. In contrast, with TLR2 ligand stimulation, TNFalpha production was reduced, while IL-6 levels, and p38 and ERK1/2 activation were not affected. In conclusion, acute ethanol exposure impaired macrophage responsiveness to multiple TLR agonists by inhibiting IL-6 and TNFalpha production. The mechanism responsible for ethanol-induced suppression involved inhibition of p38 and ERK1/2 activation. Furthermore, different TLRs mediated IL-6 and TNFalpha production via signaling pathways that showed unique characteristics.

ISBN: 0542114658Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Acute ethanol exposure inhibits toll-like receptor-mediated inflammatory responses of murine macrophages.
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245 1 0 $a Acute ethanol exposure inhibits toll-like receptor-mediated inflammatory responses of murine macrophages.
300 $a 156 p.
500 $a Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2497.
500 $a Director: Elizabeth J. Kovacs.
502 $a Thesis (Ph.D.)--Loyola University Chicago, 2005.
520 $a Ethanol is known to increase susceptibility to infections, in part, by suppressing macrophage function. Through toll-like receptors (TLRs), macrophages recognize pathogens and initiate inflammatory responses. In this study, the effect of acute ethanol exposure on murine macrophage activation mediated via TLR2, TLR4 and TLR9 was investigated. Specifically, the study focused on the pro-inflammatory cytokines IL-6 and TNFalpha and activation of p38 and ERK1/2 mitogen-activated protein kinases (MAPKs) after a single in vivo exposure to physiologically relevant level of ethanol followed by ex vivo stimulation with specific TLR ligands. Acute ethanol treatment inhibited IL-6 and TNFalpha synthesis 3 and 24 hours after administration and impaired p38 and ERK1/2 activation induced by TLR2, TLR4, and TLR9 ligands. We also addressed the question of whether ethanol treatment modified activities of serine/threonine-specific, tyrosine-specific phosphatases, and MAPK phosphatase-1. Inhibitors of three families of protein phosphatases did not restore ethanol-impaired pro-inflammatory cytokines production nor p38 and ERK1/2 activation. However, inhibitors of ser/thr protein phosphatase-type I and -2A (PP1, PP2A) significantly increased IL-6 and TNFalpha levels, and prolonged activation of p38 and ERK1/2 when triggered by TLR4 and TLR9 ligands. In contrast, with TLR2 ligand stimulation, TNFalpha production was reduced, while IL-6 levels, and p38 and ERK1/2 activation were not affected. In conclusion, acute ethanol exposure impaired macrophage responsiveness to multiple TLR agonists by inhibiting IL-6 and TNFalpha production. The mechanism responsible for ethanol-induced suppression involved inhibition of p38 and ERK1/2 activation. Furthermore, different TLRs mediated IL-6 and TNFalpha production via signaling pathways that showed unique characteristics.
590 $a School code: 0112.
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