Document Detail


Febrile-range hyperthermia augments lipopolysaccharide-induced lung injury by a mechanism of enhanced alveolar epithelial apoptosis.
MedLine Citation:
PMID:  20200273     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fever is common in critically ill patients and is associated with worse clinical outcomes, including increased intensive care unit mortality. In animal models, febrile-range hyperthermia (FRH) worsens acute lung injury, but the mechanisms by which this occurs remain uncertain. We hypothesized that FRH augments the response of the alveolar epithelium to TNF-alpha receptor family signaling. We found that FRH augmented LPS-induced lung injury and increased LPS-induced mortality in mice. At 24 h, animals exposed to hyperthermia and LPS had significant increases in alveolar permeability without changes in inflammatory cells in bronchoalveolar lavage fluid or lung tissue as compared with animals exposed to LPS alone. The increase in alveolar permeability was associated with an increase in alveolar epithelial apoptosis and was attenuated by caspase inhibition with zVAD.fmk. At 48 h, the animals exposed to hyperthermia and LPS had an enhanced lung inflammatory response. In murine lung epithelial cell lines (MLE-15, LA-4) and in primary type II alveolar epithelial cells, FRH enhanced apoptosis in response to TNF-alpha but not Fas ligand. The increase in apoptosis was caspase-8 dependent and associated with suppression of NF-kappaB activity. The FRH-associated NF-kappaB suppression was not associated with persistence of IkappaB-alpha, suggesting that FRH-mediated suppression of NF-kappaB occurs by means other than alteration of IkappaB-alpha kinetics. These data show for the first time that FRH promotes lung injury in part by increasing lung epithelial apoptosis. The enhanced apoptotic response might relate to FRH-mediated suppression of NF-kappaB activity in the alveolar epithelium with a resultant increase in susceptibility to TNF-alpha-mediated cell death.
Authors:
Anne B Lipke; Gustavo Matute-Bello; Raquel Herrero; Kiyoyasu Kurahashi; Venus A Wong; Stephen M Mongovin; Thomas R Martin
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-03-03
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  184     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-03-22     Completed Date:  2010-04-27     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3801-13     Citation Subset:  AIM; IM    
Affiliation:
Medical Research Service, VA Puget Sound Medical Center, University of Washington, Seattle, WA 98108, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology*
Bronchoalveolar Lavage Fluid / chemistry
Epithelial Cells / pathology
Fever / immunology,  physiopathology*
Flow Cytometry
In Situ Nick-End Labeling
Inflammation / immunology,  physiopathology
Lipopolysaccharides / immunology,  toxicity
Lung Injury / immunology,  physiopathology*
Male
Mice
Mice, Inbred C57BL
NF-kappa B / metabolism
Pulmonary Alveoli / immunology,  pathology*
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction
Tumor Necrosis Factor-alpha / metabolism
Grant Support
ID/Acronym/Agency:
F32 HL096348-01/HL/NHLBI NIH HHS; HL081764/HL/NHLBI NIH HHS; HL083044/HL/NHLBI NIH HHS; HL096348/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Lipopolysaccharides; 0/NF-kappa B; 0/Tumor Necrosis Factor-alpha
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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