PMID- 16220077
OWN - NLM
STAT- MEDLINE
DCOM- 20060302
LR  - 20190724
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 46
IP  - 5
DP  - 2005 Nov
TI  - C-reactive protein augments interleukin-8 secretion in human peripheral blood 
      monocytes.
PG  - 690-6
AB  - C-reactive protein (CRP) is a powerful predictor and risk factor for 
      cardiovascular diseases. The CXC- and CC-type chemokines interleukin-8 (IL-8) and 
      monocyte chemoattractant protein-1 (MCP-1) are important chemokines for leukocyte 
      trafficking identified in atheromatous plaque expressed mainly by macrophages in 
      humans. We assessed whether C-reactive protein could induce MCP-1 and IL-8 
      secretion. In human peripheral blood monocytes, C-reactive protein (12.5-50 
      microg/mL) increased IL-8, but not MCP-1 secretion in a time- (6-24 hours) and 
      dose-dependent manner as detected by ELISA. C-reactive protein could augment the 
      production of reactive oxygen species (ROS) as measured by chemiluminescence and 
      inhibitors of NAD(P)H oxidase (DPI and PAO) and ROS scavengers (superoxide 
      dismutase, catalase, and 1% dimethyl sulphoxide) abolished C-reactive 
      protein-induced IL-8 secretion. Furthermore, relative quantity of IL-8 mRNA was 
      significantly increased by C-reactive protein 50 microg/mLfor 12 hours, which 
      could be inhibited by DPI 1 microM or superoxide dismutase (SOD) 250 U/mL. The 
      inhibitors of ERK 1/2 (PD98059), p38 (SB203580) MAPK, and NF-kappaB (PDTC and 
      MG132) significantly decreased C-reactive protein-induced IL-8 secretion in human 
      monocytes. Also, agonists of peroxisome proliferator-activated receptor (PPAR) 
      alpha (WY14643) and PPARgamma (troglitazone) could largely inhibit C-reactive 
      protein responses. Thus, our data indicate that C-reactive protein at pathologic 
      levels increases IL-8 secretion and mRNA via enhancing ROS derived mainly from 
      NAD(P)H oxidase and the subsequent activation of ERK1/2, p38 MAPK, and NF-kappaB. 
      The activation of PPARalpha/gamma can negatively regulate C-reactive 
      protein-induced IL-8 production in human monocytes.
FAU - Xie, Liangqi
AU  - Xie L
AD  - Department of Physiology and Key Laboratory of Molecular Cardiovascular Science 
      of Education Ministry, Basic Medical College, Peking University, Beijing 100-083, 
      China.
FAU - Chang, Lina
AU  - Chang L
FAU - Guan, Youfei
AU  - Guan Y
FAU - Wang, Xian
AU  - Wang X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-8)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Recombinant Proteins)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - C-Reactive Protein/*pharmacology
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Humans
MH  - Interleukin-8/*metabolism
MH  - Monocytes/*drug effects/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Recombinant Proteins/*pharmacology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Time Factors
EDAT- 2005/10/13 09:00
MHDA- 2006/03/03 09:00
CRDT- 2005/10/13 09:00
PHST- 2005/10/13 09:00 [pubmed]
PHST- 2006/03/03 09:00 [medline]
PHST- 2005/10/13 09:00 [entrez]
AID - 00005344-200511000-00017 [pii]
AID - 10.1097/01.fjc.0000183568.48389.a1 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 2005 Nov;46(5):690-6. doi: 
      10.1097/01.fjc.0000183568.48389.a1.