Toll-like receptor and tumour necrosis factor dependent endotoxin-induced acute lung injury.

Toll-like receptor and tumour necrosis factor dependent endotoxin-induced acute lung injury. Research Abstract Details 

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Toll-like receptor and tumour necrosis factor dependent endotoxin-induced acute lung injury. Abstract Text:

Togbe,Silvia Schnyder-Candrian,Bruno Schnyder,Emilie Doz,Nicolas Noulin,Laure Janot,Thomas Secher,Pamela Gasse,Carla Lima,Fernando Rodrigues Coelho,Virginie Vasseur, Erard,Bernhard Ryffel,Isabelle Couillin,Rene Moser, Togbe,Silvia Schnyder-Candrian,Bruno Schnyder,Emilie Doz,Nicolas Noulin,Laure Janot,Thomas Secher,Pamela Gasse,Carla Lima,Fernando Rodrigues Coelho,Virginie Vasseur, Erard,Bernhard Ryffel,Isabelle Couillin,Rene Moser,

Recent studies on endotoxin/lipopolysaccharide (LPS)-induced acute inflammatory response in the lung are reviewed. The acute airway inflammatory response to inhaled endotoxin is mediated through Toll-like receptor 4 (TLR4) and CD14 signalling as mice deficient for TLR4 or CD14 are unresponsive to endotoxin. Acute bronchoconstriction, tumour necrosis factor (TNF), interleukin (IL)-12 and keratinocyte-derived chemokine (KC) production, protein leak and neutrophil recruitment in the lung are abrogated in mice deficient for the adaptor molecules myeloid differentiation factor 88 (MyD88) and Toll/Interleukin-1 receptor (TIR)-domain-containing adaptor protein (TIRAP), but independent of TIR-domain-containing adaptor-inducing interferon-beta (TRIF). In particular, LPS-induced TNF is required for bronchoconstriction, but dispensable for inflammatory cell recruitment. Lipopolysaccharide induces activation of the p38 mitogen-activated protein kinase (MAPK). Inhibition of pulmonary MAPK activity abrogates LPS-induced TNF production, bronchoconstriction, neutrophil recruitment into the lungs and broncho-alveolar space. In conclusion, TLR4-mediated, bronchoconstriction and acute inflammatory lung pathology to inhaled endotoxin are dependent on TLR4/CD14/MD2 expression using the adapter proteins TIRAP and MyD88, while TRIF, IL-1R1 or IL-18R signalling pathways are dispensable. Further downstream in this axis of signalling, TNF blockade reduces only acute bronchoconstriction, while MAPK inhibition abrogates completely endotoxin-induced inflammation.

Toll-like receptor and tumour necrosis factor dependent endotoxin-induced acute lung injury. Publishing Authors By Initials

D Togbe,S Schnyder-Candrian,B Schnyder,E Doz,N Noulin,L Janot,T Secher,P Gasse,C Lima,FR Coelho,V Vasseur,F Erard,B Ryffel,I Couillin,R Moser,D Togbe,S Schnyder-Candrian,B Schnyder,E Doz,N Noulin,L Janot,T Secher,P Gasse,C Lima,FR Coelho,V Vasseur,F Erard,B Ryffel,I Couillin,R Moser,

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Toll-like receptor and tumour necrosis factor dependent endotoxin-induced acute lung injury. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: International journal of experimental pathology

VOLUME: 88

Page Numbers: 387-91

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ISSN: 1365-2613

DAY: 27

MONTH: Dec

YEAR: 2007

Toll-like receptor and tumour necrosis factor dependent endotoxin-induced acute lung injury. Information

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LANGUAGE: eng

NlmUniqueID: 9014042

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Grant and Affiliation Information for Toll-like receptor and tumour necrosis factor dependent endotoxin-induced acute lung injury.

AFFILIATION: Molecular Immunology and Embryology, University of Orléans and CNRS UMR6218, Transgenose Institute, Orleans, France.

Country: England

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MEDLINETA: Int J Exp Pathol

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