PMID- 14733721
OWN - NLM
STAT- MEDLINE
DCOM- 20040816
LR  - 20071115
IS  - 0968-0519 (Print)
IS  - 0968-0519 (Linking)
VI  - 9
IP  - 6
DP  - 2003
TI  - Effects of bacterial cell wall components (PAMPs) on the expression of monocyte 
      chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1alpha 
      (MIP-1alpha) and the chemokine receptor CCR2 by purified human blood monocytes.
PG  - 349-60
AB  - Regulation of chemokine production and the expression of chemokine receptors play 
      an important role during inflammation and infectious diseases. The present study 
      was designed to study the effects of five different bacterial cell wall 
      components (PAMPs) on the production of MCP-1 and MIP-1alpha and the expression 
      of CCR2 by highly purified human blood monocytes. All five PAMPs induced high 
      expression of mRNA and protein synthesis of both chemokines. Generally, MCP-1 
      mRNA and protein levels were higher than MIP-1alpha levels. Expression of MCP-1 
      and MIP-1alpha differed both at the mRNA and at the protein levels, MIP-1alpha 
      always showing a more rapid initial increase, attaining lower protein levels than 
      MCP-1. Antibodies against CD14 significantly inhibited the inducing effects of 
      all the PAMPs used. Antibody against TLR2 inhibited the chemokine production 
      induced by LTA and AraLAM by more than 36% (P < 0.05) while chemokine production 
      induced by Escherichia coli-LPS, purified E. coli-LPS and Neisseria 
      meningitidis-LPS was inhibited by more than 60% by antibody against TLR4 (P < 
      0.05). The inducing effects of all five PAMPs could be inhibited by rIL-4, rIL-10 
      and rIL-13. rIL-4 was the most effective. Generally, IC(50) of these 
      anti-inflammatory cytokines were lower for the MIP-1alpha than for the MCP-1 
      production. The cell surface expression of CCR2 was significantly down-regulated 
      by all five PAMPs in addition to a decrease in cytosolic free calcium and binding 
      of rMCP-1. We conclude that MCP-1 and MIP-1alpha as well as the MCP-1 receptor 
      CCR2 will be substantially regulated upon monocyte contact with various cell wall 
      components (PAMPs) from Gram-negative and Gram-positive bacteria as well as from 
      mycobacteria.
FAU - Moller, Anne-Sophie W
AU  - Moller AS
AD  - Department of Clinical Chemistry, The Research and Development Group, Ullevaal 
      University Hospital, N-0450 Oslo, Norway. a.s.w.moller@ioks.uio.no
FAU - Ovstebo, Reidun
AU  - Ovstebo R
FAU - Westvik, Ase-Brit
AU  - Westvik AB
FAU - Joo, Gun Britt
AU  - Joo GB
FAU - Haug, Kari-Bente F
AU  - Haug KB
FAU - Kierulf, Peter
AU  - Kierulf P
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Endotoxin Res
JT  - Journal of endotoxin research
JID - 9433350
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (Recombinant Proteins)
SB  - IM
MH  - Antibodies, Monoclonal/metabolism
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Cytokines/pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Gram-Negative Bacteria/chemistry
MH  - Gram-Positive Bacteria/chemistry
MH  - Humans
MH  - Limulus Test
MH  - Lipopolysaccharides/*pharmacology
MH  - Macrophage Inflammatory Proteins/genetics/*metabolism
MH  - Monocytes/drug effects/*metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Receptors, Chemokine/*metabolism
MH  - Recombinant Proteins/metabolism
EDAT- 2004/01/22 05:00
MHDA- 2004/08/18 05:00
CRDT- 2004/01/22 05:00
PHST- 2004/01/22 05:00 [pubmed]
PHST- 2004/08/18 05:00 [medline]
PHST- 2004/01/22 05:00 [entrez]
AID - 10.1179/096805103225002791 [doi]
PST - ppublish
SO  - J Endotoxin Res. 2003;9(6):349-60. doi: 10.1179/096805103225002791.