Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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Originally published online as doi:10.1189/jlb.0405236 on October 21, 2005

Published online before print October 21, 2005
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(Journal of Leukocyte Biology. 2005;78:1301-1305.)
© 2005 by Society for Leukocyte Biology

Endotoxin tolerance induces selective alterations in neutrophil function

Lisa C. Parker*,1, 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

1 Correspondence: Academic Unit of Respiratory Medicine, Division of Genomic Medicine, University of Sheffield, M Floor, Royal Hallamshire Hospital, Sheffield, S10 2JF, UK. E-mail: l.c.parker{at}sheffield.ac.uk

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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