PMID- 10092818
OWN - NLM
STAT- MEDLINE
DCOM- 19990413
LR  - 20061115
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 162
IP  - 6
DP  - 1999 Mar 15
TI  - Modulation of formyl peptide receptor expression by IL-10 in human monocytes and 
      neutrophils.
PG  - 3590-5
AB  - IL-10, originally described as a cytokine synthesis inhibitory factor, is
      secreted by a number of cells of the immune system, including monocytes and T
      cells. Although IL-10 is being assigned as an immunosuppressive cytokine, our
      study showed that FMLP-R mRNA was rapidly up-regulated by exposure of monocytes
      to graded concentrations of this cytokine, with maximal (three- to fourfold)
      stimulation with 10 ng/ml. The effect was rapid, being observable as early as 1 h
      of treatment with IL-10, maximal between 2 and 4 h, and still evident after 24 h 
      and was associated with an increase of receptor expression on the cell surface as
      assessed by flow cytometry analysis. Pretreatment of monocytes with actinomycin D
      completely abrogated the effect of IL-10, suggesting a transcriptional
      regulation. Moreover, IL-10-treated monocytes showed a significantly enhanced
      functional responsiveness to FMLP with enhanced (three- to fourfold) chemotaxis
      and augmented (twofold) intracellular calcium mobilization. In polymorphonuclear 
      neutrophils (PMN), IL-10 also mediated a twofold augmentation of FMLP-R
      expression. In parallel experiments, we observed that IL-10 could differentially 
      modulate other chemotactic receptors. Hence, we observed that IL-10 augmented
      two-to threefold platelet-activating factor receptor (PAF-R) expression, whereas 
      it had no significant effect on the fifth component of complement (C5a) receptor 
      (C5a-R) expression. Collectively, our results demonstrate that IL-10 may play an 
      important role in inflammatory process through modulation of chemotactic receptor
      expression.
FAU - Thivierge, M
AU  - Thivierge M
AD  - Department of Pediatrics, Faculty of Medicine, Universite de Sherbrooke, Quebec, 
      Canada.
FAU - Parent, J L
AU  - Parent JL
FAU - Stankova, J
AU  - Stankova J
FAU - Rola-Pleszczynski, M
AU  - Rola-Pleszczynski M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Formyl Peptide)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Receptors, Peptide)
RN  - 130068-27-8 (Interleukin-10)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
SB  - AIM
SB  - IM
MH  - Chemotaxis, Leukocyte/immunology
MH  - Gene Expression Regulation/immunology
MH  - Humans
MH  - Interleukin-10/*physiology
MH  - Monocytes/immunology/*metabolism/physiology
MH  - N-Formylmethionine Leucyl-Phenylalanine/*metabolism/pharmacology
MH  - Neutrophils/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Receptors, Formyl Peptide
MH  - Receptors, Immunologic/*biosynthesis/genetics
MH  - Receptors, Peptide/*biosynthesis/genetics
MH  - Transcription, Genetic/immunology
MH  - Up-Regulation/immunology
EDAT- 1999/03/27 00:00
MHDA- 1999/03/27 00:01
CRDT- 1999/03/27 00:00
PHST- 1999/03/27 00:00 [pubmed]
PHST- 1999/03/27 00:01 [medline]
PHST- 1999/03/27 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1999 Mar 15;162(6):3590-5.