MONOCYTE CHEMOATTRACTANT PROTEIN-1 AND INTERLEUKIN-8 PRODUCTION IN MONONUCLEAR-CELLS STIMULATED BY ORAL MICROORGANISMS

Citation
Yl. Jiang et al., MONOCYTE CHEMOATTRACTANT PROTEIN-1 AND INTERLEUKIN-8 PRODUCTION IN MONONUCLEAR-CELLS STIMULATED BY ORAL MICROORGANISMS, Infection and immunity, 64(11), 1996, pp. 4450-4455
Citations number
28
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
64
Issue
11
Year of publication
1996
Pages
4450 - 4455
Database
ISI
SICI code
0019-9567(1996)64:11<4450:MCPAIP>2.0.ZU;2-U
Abstract
Chemokines are a family of low-molecular-weight proinflammatory cytoki nes that stimulate recruitment of leukocytes. The chemokines interleuk in-8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1) are relativ ely specific chemoattractants for neutrophils and monocytes, respectiv ely. Chemokine expression contributes to the presence of different leu kocyte populations observed in normal and pathologic states. In the pr esent studied, peripheral blood mononuclear cells (PBMC) were stimulat ed by microbes (Candida albicans, Streptococcus mutans, Porphyromonas gingivalis, and Actinobacillus actinomycetemcomitans) selected based u pon their importance as oral pathogens. IL-8 and MCP-1 gene expression and protein release were determined by Northern blot (RNA blot) analy sis and enzyme-linked immunosorbent assay. C. albicans, P. gingivalis, and A. actinomycetemcomitans induced high levels of production of bot h 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 vers us IL-8, differences in the effects of various microbe concentrations were observed only for A. actinomycetemcomitans. These results demonst rate that different oral pathogens induce specific dose-dependent patt erns of chemokine gene expression and release. Such patterns may help explain the immunopathology of oral infections, particularly with rega rd to inflammatory leukocyte recruitment.