Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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A more recent version of this article appeared on December 1, 2005

Published online before print October 21, 2005
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0405236

Received for publication April 29, 2005.
Revised August 12, 2005.
Accepted for publication September 8, 2005.

Article

Endotoxin tolerance induces selective alterations in neutrophil function

Lisa C. Parker *@, Elizabeth C. Jones *, Lynne R. Prince *, Steven K. Dower {dagger}, Moira K. B. Whyte *, and Ian Sabroe *

Academic Units of *Respiratory Medicine and {dagger}Cell Biology, Section of Functional Genomics, Division of Genomic Medicine, University of Sheffield, United Kingdom

@ To whom correspondence should be addressed. E-mail: l.c.parker{at}sheffield.ac.uk.


  Abstract

Endotoxin tolerance has the potential to limit phagocyte responses to Toll-like receptor (TLR) agonists, but the role of tolerance in regulating neutrophil responses is unknown. We investigated neutrophil responses to prolonged lipopolysaccharide (LPS) exposure and observed induction of tolerance in intracellular signaling pathways and respiratory burst. These effects were not prevented by granulocyte macrophage-colony stimulating factor (GM-CSF) pretreatment, and tolerized neutrophils retained the ability to respond to GM-CSF and other survival factors with a delay in apoptosis. In addition, LPS-exposed neutrophils showed continued generation of CXC chemokine ligand 8, which was not reduced in tolerized cells. Induction of tolerance was associated with a loss of TLR4 surface expression. Tolerance, therefore, induces a selective reprogramming of neutrophil function, but cells retain a predominantly proinflammatory phenotype.

Key Words: inflammation • LPS • TLR




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