Journal of Leukocyte Biology
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Published online before print September 14, 2006
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0206086

Received for publication February 7, 2006.
Revised July 11, 2006.
Accepted for publication August 4, 2006.

Article

Vasoactive intestinal peptide inhibits up-regulation of human monocyte TLR2 and TLR4 by LPS and differentiation of monocytes to macrophages

N. Foster , S. R. Lea , P. M. Preshaw , and J. J. Taylor @

Oral Microbiology and Host Responses Group, Oral Biology, School of Dental Sciences, University of Newcastle upon Tyne, United Kingdom

@ To whom correspondence should be addressed. E-mail: j.j.taylor{at}ncl.ac.uk.


  Abstract

Vasoactive intestinal peptide (VIP) is an immunoregulatory peptide, which inhibits LPS-induced cytokine secretion in myeloid cells and has beneficial effects in animal models of inflammatory diseases. We show for the first time that VIP decreases LPS-induced up-regulation of TLR2 and TLR4 by human monocytic THP1 cells and peripheral blood monocytes (PBM). VIP inhibited up-regulation of TLR4 expression in THP1 cells in response to LPS from Escherichia coli or the periodontal pathogen Porphyromonas gingivalis within 6 h poststimulation but had less of an effect on TLR2. After 24 h, P. gingivalis LPS stimulated monocytic THP1 cells to differentiate into macrophages, which predominantly expressed TLR2, and E. coli LPS-stimulated THP1 differentiation to predominantly TLR4-expressing macrophages. VIP decreased monocyte differentiation to macrophages induced by LPS from either species and also reduced overall TLR2 and TLR4 expression in these cells. VIP had a similar effect on human PBM. The transcription factor PU.1 regulates TLR expression and has a central role in myeloid cell differentiation. VIP inhibited the nuclear translocation of PU.1 in LPS-stimulated THP-1 monocytes. VIP also inhibited the expression of the M-CSF receptor, which is regulated by PU.1. In summary, VIP inhibited LPS-induced differentiation of monocytes with a concomitant reduction in TLR2 and TLR4 expression. Although there was differential induction of TLR expression by LPS from P. gingivalis and E. coli, VIP inhibited the action of both of these LPS types on monocytes. The mechanism of action of VIP on monocyte differentiation may be via inhibition of the transcription factor PU.1.

Key Words: VIP • myeloid cells • Toll-like receptors • lipopolysaccharide




This article has been cited by other articles:


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 J. Dent. Res.Home page
N. Foster, K. Andreadou, L. Jamieson, P.M. Preshaw, and J.J. Taylor
VIP Inhibits P. gingivalis LPS-induced IL-18 and IL-18BPa in Monocytes
J. Dent. Res., September 1, 2007; 86(9): 883 - 887.
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