PMID- 8890191
OWN - NLM
STAT- MEDLINE
DCOM- 19970106
LR  - 20210526
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 64
IP  - 11
DP  - 1996 Nov
TI  - Monocyte chemoattractant protein 1 and interleukin-8 production in mononuclear 
      cells stimulated by oral microorganisms.
PG  - 4450-5
AB  - Chemokines are a family of low-molecular-weight proinflammatory cytokines that 
      stimulate recruitment of leukocytes. The chemokines interleukin-8 (IL-8) and 
      monocyte chemoattractant protein 1 (MCP-1) are relatively specific 
      chemoattractants for neutrophils and monocytes, respectively. Chemokine 
      expression contributes to the presence of different leukocyte populations 
      observed in normal and pathologic states. In the present studies, peripheral 
      blood mononuclear cells (PBMC) were stimulated by microbes (Candida albicans, 
      Streptococcus mutans, Porphyromonas gingivalis, and Actinobacillus 
      actinomycetemcomitans) selected based upon their importance as oral pathogens. 
      IL-8 and MCP-1 gene expression and protein release were determined by Northern 
      blot (RNA blot) analysis and enzyme-linked immunosorbent assay. C. albicans, P. 
      gingivalis, and A. actinomycetemcomitans induced high levels of production of 
      both MCP-1 and IL-8. S. mutans was a strong inducer of MCP-1, but it did not 
      stimulate significant production of IL-8. C. albicans, S. mutans, and A. 
      actinomycetemcomitans were 500 to 5,000 times more potent than P. gingivalis in 
      terms of MCP-1 production. In general, the microbe-to-PBMC ratios required for 
      maximum gene expression of MCP-1 were lower than those for IL-8. However, for 
      actual protein release of MCP-1 versus IL-8, differences in the effects of 
      various microbe concentrations were observed only for A. actinomycetemcomitans. 
      These results demonstrate that different oral pathogens induce specific 
      dose-dependent patterns of chemokine gene expression and release. Such patterns 
      may help explain the immunopathology of oral infections, particularly with regard 
      to inflammatory leukocyte recruitment.
FAU - Jiang, Y
AU  - Jiang Y
AD  - The Evans Memorial Department of Clinical Research and the Department of 
      Medicine, Boston University Medical Center Hospital and Boston City Hospital, 
      Massachusetts 02118, USA.
FAU - Russell, T R
AU  - Russell TR
FAU - Graves, D T
AU  - Graves DT
FAU - Cheng, H
AU  - Cheng H
FAU - Nong, S H
AU  - Nong SH
FAU - Levitz, S M
AU  - Levitz SM
LA  - eng
GR  - AI25780/AI/NIAID NIH HHS/United States
GR  - DE05642/DE/NIDCR NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-8)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Aggregatibacter actinomycetemcomitans/immunology
MH  - Bacteria/*immunology
MH  - Candida albicans/*immunology
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Gene Expression Regulation
MH  - Humans
MH  - Interleukin-8/*biosynthesis/genetics
MH  - Kinetics
MH  - Leukocytes, Mononuclear/*immunology
MH  - Mouth/*microbiology
MH  - Porphyromonas gingivalis/immunology
MH  - RNA, Messenger/biosynthesis/genetics
MH  - Species Specificity
MH  - Streptococcus mutans/immunology
PMC - PMC174397
EDAT- 1996/11/01 00:00
MHDA- 1996/11/01 00:01
PMCR- 1996/11/01
CRDT- 1996/11/01 00:00
PHST- 1996/11/01 00:00 [pubmed]
PHST- 1996/11/01 00:01 [medline]
PHST- 1996/11/01 00:00 [entrez]
PHST- 1996/11/01 00:00 [pmc-release]
AID - 10.1128/iai.64.11.4450-4455.1996 [doi]
PST - ppublish
SO  - Infect Immun. 1996 Nov;64(11):4450-5. doi: 10.1128/iai.64.11.4450-4455.1996.