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TLR4 signaling-induced heme oxygenase upregulation in the acute lung injury: role in hemorrhagic shock and two-hit induced lung inflammation

Resuscitated hemorrhagic shock is believed to promote the development of acute lung injury (ALI) by priming the immune system for an exaggerated inflammatory response to a second trivial stimulus. This work explored effects of TLR4 on hemorrhage-induced ALI and “second-hit” responses, and further ex... Full description

Journal Title: Molecular Biology Reports 2013, Vol.40(2), pp.1167-1172
Main Author: Chen, Chang
Other Authors: Zhang, Fan , Zhang, Zongze , Peng, Mian , Wang, Yanlin , Chen, Yingying
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0301-4851 ; E-ISSN: 1573-4978 ; DOI: 10.1007/s11033-012-2158-y
Link: http://dx.doi.org/10.1007/s11033-012-2158-y
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recordid: springer_jour10.1007/s11033-012-2158-y
title: TLR4 signaling-induced heme oxygenase upregulation in the acute lung injury: role in hemorrhagic shock and two-hit induced lung inflammation
format: Article
creator:
  • Chen, Chang
  • Zhang, Fan
  • Zhang, Zongze
  • Peng, Mian
  • Wang, Yanlin
  • Chen, Yingying
subjects:
  • Hemorrhagic shock
  • Acute lung injury
  • Lipopolysaccharide
  • Toll-like receptor4
  • Inducible heme oxygenase
ispartof: Molecular Biology Reports, 2013, Vol.40(2), pp.1167-1172
description: Resuscitated hemorrhagic shock is believed to promote the development of acute lung injury (ALI) by priming the immune system for an exaggerated inflammatory response to a second trivial stimulus. This work explored effects of TLR4 on hemorrhage-induced ALI and “second-hit” responses, and further explore the mechanisms involved in “second-hit” responses. Expression of HO-1, IL-10, lung W/D and MPO markedly increased at nearly all time-points examined in HSR/LPS group as compared with sham/LPS group in WT mice. In HSR/LPS mice, the induced amount of IL-10 and the expressions of HO-1 of WT mice were significantly higher compared with TLR-4d/d. This study provides in vivo evidence that pulmonary infections after LPS instillation contribute to local tissue release of pro-inflammatory mediators after HSR systemic. Activation of TLR4 might induce HO-1 expression and HO-1 modulates proinflammatory responses that are triggered via TLR4 signaling.
language: eng
source:
identifier: ISSN: 0301-4851 ; E-ISSN: 1573-4978 ; DOI: 10.1007/s11033-012-2158-y
fulltext: fulltext
issn:
  • 1573-4978
  • 15734978
  • 0301-4851
  • 03014851
url: Link


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titleTLR4 signaling-induced heme oxygenase upregulation in the acute lung injury: role in hemorrhagic shock and two-hit induced lung inflammation
creatorChen, Chang ; Zhang, Fan ; Zhang, Zongze ; Peng, Mian ; Wang, Yanlin ; Chen, Yingying
ispartofMolecular Biology Reports, 2013, Vol.40(2), pp.1167-1172
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subjectHemorrhagic shock ; Acute lung injury ; Lipopolysaccharide ; Toll-like receptor4 ; Inducible heme oxygenase
descriptionResuscitated hemorrhagic shock is believed to promote the development of acute lung injury (ALI) by priming the immune system for an exaggerated inflammatory response to a second trivial stimulus. This work explored effects of TLR4 on hemorrhage-induced ALI and “second-hit” responses, and further explore the mechanisms involved in “second-hit” responses. Expression of HO-1, IL-10, lung W/D and MPO markedly increased at nearly all time-points examined in HSR/LPS group as compared with sham/LPS group in WT mice. In HSR/LPS mice, the induced amount of IL-10 and the expressions of HO-1 of WT mice were significantly higher compared with TLR-4d/d. This study provides in vivo evidence that pulmonary infections after LPS instillation contribute to local tissue release of pro-inflammatory mediators after HSR systemic. Activation of TLR4 might induce HO-1 expression and HO-1 modulates proinflammatory responses that are triggered via TLR4 signaling.
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titleTLR4 signaling-induced heme oxygenase upregulation in the acute lung injury: role in hemorrhagic shock and two-hit induced lung inflammation
descriptionResuscitated hemorrhagic shock is believed to promote the development of acute lung injury (ALI) by priming the immune system for an exaggerated inflammatory response to a second trivial stimulus. This work explored effects of TLR4 on hemorrhage-induced ALI and “second-hit” responses, and further explore the mechanisms involved in “second-hit” responses. Expression of HO-1, IL-10, lung W/D and MPO markedly increased at nearly all time-points examined in HSR/LPS group as compared with sham/LPS group in WT mice. In HSR/LPS mice, the induced amount of IL-10 and the expressions of HO-1 of WT mice were significantly higher compared with TLR-4d/d. This study provides in vivo evidence that pulmonary infections after LPS instillation contribute to local tissue release of pro-inflammatory mediators after HSR systemic. Activation of TLR4 might induce HO-1 expression and HO-1 modulates proinflammatory responses that are triggered via TLR4 signaling.
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abstractResuscitated hemorrhagic shock is believed to promote the development of acute lung injury (ALI) by priming the immune system for an exaggerated inflammatory response to a second trivial stimulus. This work explored effects of TLR4 on hemorrhage-induced ALI and “second-hit” responses, and further explore the mechanisms involved in “second-hit” responses. Expression of HO-1, IL-10, lung W/D and MPO markedly increased at nearly all time-points examined in HSR/LPS group as compared with sham/LPS group in WT mice. In HSR/LPS mice, the induced amount of IL-10 and the expressions of HO-1 of WT mice were significantly higher compared with TLR-4d/d. This study provides in vivo evidence that pulmonary infections after LPS instillation contribute to local tissue release of pro-inflammatory mediators after HSR systemic. Activation of TLR4 might induce HO-1 expression and HO-1 modulates proinflammatory responses that are triggered via TLR4 signaling.
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doi10.1007/s11033-012-2158-y
pages1167-1172
date2013-02