Extracellular heat shock protein-70 induces endotoxin tolerance in THP-1 cells.

Extracellular heat shock protein-70 induces endotoxin tolerance in THP-1 cells. Research Abstract Details 

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Extracellular heat shock protein-70 induces endotoxin tolerance in THP-1 cells. Abstract Text:

Rajesh Aneja,Kelli Odoms,Katherine Dunsmore,Thomas P Shanley,Hector R Wong,

Recent data suggest that heat shock protein-70 (HSP-70), an intracellular protein, can exist in the extracellular compartment and signal through the CD14/TLR4 pathway. In this study, we tested the hypothesis that extracellular HSP-70 induces endotoxin (LPS) tolerance. Using human monocyte cell line (THP-1), initial dose-response experiments were conducted to determine a subthreshold concentration of HSP-70 that does not induce NF-kappaB activity. Differentiated THP-1 cells were preconditioned with subthreshold concentration (0.03 microg/ml HSP-70) for 18 h, followed by LPS stimulation (1 microg/ml) for 4 h. Preconditioning with HSP-70 decreased subsequent LPS-mediated NF-kappaB-dependent promoter activity and was accompanied by significant decreases of supernatant TNF levels. Furthermore, human monocytes isolated from human volunteers, subsequently preconditioned with HSP-70, demonstrated LPS tolerance as evidenced by abrogated supernatant TNF levels. Additional experiments were conducted to exclude the possibility of endotoxin contamination of HSP-70 by boiling HSP-70 at 100 degrees C for 1 h or preconditioning with equivalent concentrations of endotoxin as present in the HSP-70 preparation. These experiments indicated that induction of tolerance was not secondary to endotoxin contamination. Neutralization experiments with an anti-HSP-70 Ab confirmed the specificity of HSP-70 in tolerance induction. Preconditioning with HSP-70 attenuated cytosolic degradation of inhibitor kappaB-alpha and inhibited activation of inhibitor kappaB kinase following LPS stimulation. HSP-70 preconditioning decreased phosphorylation of the p65 subunit of NF-kappaB following LPS stimulation. These data suggest a novel role for extracellular HSP-70 in modifying mononuclear cell responses to subsequent LPS challenge.

Extracellular heat shock protein-70 induces endotoxin tolerance in THP-1 cells. Publishing Authors By Initials

R Aneja,K Odoms,K Dunsmore,TP Shanley,HR Wong,

For similar peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research

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Extracellular heat shock protein-70 induces endotoxin tolerance in THP-1 cells. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 177

Page Numbers: 7184-92

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 15

MONTH: Nov

YEAR: 2006

Extracellular heat shock protein-70 induces endotoxin tolerance in THP-1 cells. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985117

Extracellular heat shock protein-70 induces endotoxin tolerance in THP-1 cells. Keywords Mesh Terms:

KEYWORDS: Tumor Necrosis Factor-alpha

MESH TERMS: metabolism

Chemical & Substance for Abstract: Extracellular heat shock protein-70 induces endotoxin tolerance in THP-1 cells. Information

Substance Name: Tumor Necrosis Factor-alpha

Registry Number: 0

Grant and Affiliation Information for Extracellular heat shock protein-70 induces endotoxin tolerance in THP-1 cells.

AFFILIATION: Department of Critical Care Medicine, University of Pittsburgh School of Medicine and Children's Hospital of Pittsburgh, Pittsburgh, PA 15213, USA. anejar@upmc.edu

Country: United States

AGENCY: United States NIGMS

GRANT: R01GM66839

ACRONYM: GM

MEDLINETA: J Immunol

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