PMID- 16367933
OWN - NLM
STAT- MEDLINE
DCOM- 20060206
LR  - 20181113
IS  - 0009-9104 (Print)
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Linking)
VI  - 143
IP  - 1
DP  - 2006 Jan
TI  - Porphyromonas gingivalis-induced inflammatory mediator profile in an ex vivo 
      human whole blood model.
PG  - 50-7
AB  - Periodontitis is characterized by an accumulation of inflammatory cells in 
      periodontal tissue and subgingival sites. Leukocytes play a major role in the 
      host response to Porphyromonas gingivalis, a major aetiological agent of chronic 
      periodontitis. Secretion of high levels of inflammatory mediators, including 
      cytokines and prostaglandins, by leucocytes is believed to contribute to 
      periodontal tissue destruction. The aim of this study was to investigate the 
      inflammatory response of an ex vivo whole blood model to P. gingivalis 
      stimulation. The production of interleukin-1 beta (IL-1beta), IL-4, IL-5, IL-6, 
      IL-8, IL-10, IL-12p70, IL-13, tumour necrosis factor alpha (TNF-alpha), 
      interferon gamma (IFN-gamma), IFN-gamma-inducible protein 10 (IP-10), monocyte 
      chemoattractant protein-1 (MCP-1), Regulated on Activation Normal T cell 
      Expressed and Secreted (RANTES) and prostaglandin E2 (PGE2) were quantified by 
      enzyme-linked immunosorbent assays. P. gingivalis induced the secretion of the 
      pro-inflammatory cytokines IL-1beta, TNF-alpha, IL-6 and IFN-gamma, the 
      chemokines IL-8, RANTES and MCP-1 and the inflammatory mediator PGE2 in an ex 
      vivo human whole blood model. The secretion levels were dependent on the strain 
      and the infectious dose used. While the mediator profiles were comparable between 
      six healthy subjects, a high interindividual variability in the levels of 
      secreted mediators was observed. This study supports the view that P. gingivalis, 
      by inducing high levels of inflammatory mediators from a mixed leucocyte 
      population, can contribute to the progression of periodontitis.
FAU - Bodet, C
AU  - Bodet C
AD  - Groupe de Recherche en Ecologie Buccale, Faculte de Medecine Dentaire, Universite 
      Laval, Quebec City, Quebec, Canada.
FAU - Chandad, F
AU  - Chandad F
FAU - Grenier, D
AU  - Grenier D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (Serum Albumin)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 82115-62-6 (Interferon-gamma)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Analysis of Variance
MH  - Bacteriological Techniques/methods
MH  - Bacteroidaceae Infections/*immunology
MH  - Cells, Cultured
MH  - Chemokine CCL2/analysis
MH  - Chemokine CCL5/analysis
MH  - Cytokines/*analysis
MH  - Dinoprostone/analysis
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Humans
MH  - Interferon-gamma/analysis
MH  - Interleukin-1/analysis
MH  - Interleukin-6/analysis
MH  - Interleukin-8/analysis
MH  - Periodontitis/*immunology
MH  - Porphyromonas gingivalis/metabolism/*physiology
MH  - Serum Albumin/metabolism
MH  - Species Specificity
MH  - Tumor Necrosis Factor-alpha/analysis
PMC - PMC1809557
EDAT- 2005/12/22 09:00
MHDA- 2006/02/07 09:00
PMCR- 2007/01/01
CRDT- 2005/12/22 09:00
PHST- 2005/12/22 09:00 [pubmed]
PHST- 2006/02/07 09:00 [medline]
PHST- 2005/12/22 09:00 [entrez]
PHST- 2007/01/01 00:00 [pmc-release]
AID - CEI2956 [pii]
AID - 10.1111/j.1365-2249.2005.02956.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2006 Jan;143(1):50-7. doi: 10.1111/j.1365-2249.2005.02956.x.