PMID- 12410798
OWN - NLM
STAT- MEDLINE
DCOM- 20021213
LR  - 20190818
IS  - 0300-9475 (Print)
IS  - 0300-9475 (Linking)
VI  - 56
IP  - 5
DP  - 2002 Nov
TI  - CD14-mediated induction of interleukin-8 and monocyte chemoattractant protein-1 
      by a heat-resistant constituent of Porphyromonas gingivalis in endothelial cells.
PG  - 484-91
AB  - Viable and inactivated Porphyromonas gingivalis dose-dependently induced 
      interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) secretion in 
      human umbilical vein endothelial cells (HUVECs). The inactivated P. gingivalis, 
      in comparison with viable bacteria, tended to enhance the production of both 
      chemokines more strongly. The production of MCP-1 protein began increasing 
      immediately after stimulation by P. gingivalis, and there was a nearly linear 
      increase from 0 to 8 h of incubation, whereas IL-8 production showed a linear 
      increase between 4 and 12 h of incubation. The IL-8 and MCP-1 mRNA expressions in 
      HUVECs as determined by reverse transcriptase-polymerase chain reaction (RT-PCR) 
      or Quantikine mRNA colorimetric quantification kits were found to be enhanced by 
      P. gingivalis. Furthermore, the time courses of IL-8 and MCP-1 mRNA expressions 
      were in accordance with those of protein production. Addition of polymyxin B or 
      boiling did not weaken the stimulatory effect of P. gingivalis, which inhibited 
      the effect of Escherichia coli lipopolysaccharide (E. coli LPS) and tumour 
      necrosis factor-alpha (TNF-alpha), respectively. In contrast, the induction of 
      IL-8 and MCP-1 by P. gingivalis was significantly reduced by anti-CD14 antibody. 
      Our results suggest that some heat-stable component of P. gingivalis, including 
      LPS, may be responsible for the induction of IL-8 and MCP-1 in HUVECs by a 
      CD14-dependent mechanism. These effects might be involved in the accumulation and 
      activation of neutrophils and monocytes at an early stage of the periodontal 
      pathogenesis.
FAU - Mao, S
AU  - Mao S
AD  - Department of Bacteriology; Department of Pediatrics; and Surgical Center, 
      Faculty of Medicine, Kagoshima University, Kagoshima, Japan.
FAU - Maeno, N
AU  - Maeno N
FAU - Yoshiie, K
AU  - Yoshiie K
FAU - Matayoshi, S
AU  - Matayoshi S
FAU - Fujimura, T
AU  - Fujimura T
FAU - Oda, H
AU  - Oda H
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Scand J Immunol
JT  - Scandinavian journal of immunology
JID - 0323767
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 0 (RNA, Messenger)
RN  - J2VZ07J96K (Polymyxin B)
SB  - IM
MH  - Bacteroidaceae Infections/etiology/immunology
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Endothelium, Vascular/immunology
MH  - Gene Expression
MH  - Hot Temperature
MH  - Humans
MH  - Interleukin-8/*biosynthesis/genetics
MH  - Kinetics
MH  - Lipopolysaccharide Receptors/*metabolism
MH  - Periodontitis/etiology/immunology
MH  - Polymyxin B/pharmacology
MH  - Porphyromonas gingivalis/*immunology/*pathogenicity
MH  - RNA, Messenger/genetics/metabolism
EDAT- 2002/11/02 04:00
MHDA- 2002/12/17 04:00
CRDT- 2002/11/02 04:00
PHST- 2002/11/02 04:00 [pubmed]
PHST- 2002/12/17 04:00 [medline]
PHST- 2002/11/02 04:00 [entrez]
AID - 1163 [pii]
AID - 10.1046/j.1365-3083.2002.01163.x [doi]
PST - ppublish
SO  - Scand J Immunol. 2002 Nov;56(5):484-91. doi: 10.1046/j.1365-3083.2002.01163.x.