Chemokine expression in Porphyromonas gingivalis-specific T-cell lines.
Autologous non-T cells (monocytes and B cells) were added to Porphyromonas gingivalis-specific T cell lines established from 9 healthy adults together with P. gingivalis outer membrane antigens for 4-6, 16-18, 24 and 48 h. Flow cytometry was employed to analyze the CD4 and CD8 cells, monocytes and B cells for intracytoplasmic IP-10 (interferon-gamma inducible protein 10), MCP-1 (monocyte chemoattractant protein 1), MIP-1 alpha (macrophage inflammatory protein 1 alpha) and RANTES (regulated on activation normal T cell expressed and secreted) at the four time periods. All cell types were positive for each chemokine throughout the 48-h time period. There were significantly fewer MCP-1-positive cells compared with the other 3 chemokines. However, the percentages of MCP-1, MIP-1 alpha- and RANTES-positive CD8 cells were significantly higher than the percentages of positive CD4 cells in all cultures. IP-10-positive CD4, CD14-positive monocytes and CD19-positive B cells were predominant compared with MIP-1 alpha- and RANTES-positive cells at 24 h. In conclusion, the present study has shown that P. gingivalis-specific T cells, monocytes and B cells produce chemokines in response to P. gingivalis outer membrane antigens, IP-10 being predominant, with MCP-1 being significantly reduced in comparison with IP-10, MIP-1 alpha and RANTES. Increased percentages of CD8 cells were induced to produce chemokines in comparison with CD4 cells, indicating a more preferential action on CD8 rather than CD4 cells.
Gemmell
E
E
Immunopathology Laboratory, School of Dentistry, University of Queensland, Brisbane, Australia.
Grieco
D A
DA
Seymour
G J
GJ
D000328:Adult; D000704:Analysis of Variance; D000942:Antigens, Bacterial / Q000276:immunology*; D018941:Antigens, CD19; D001402:B-Lymphocytes / Q000378:metabolism; D001425:Bacterial Outer Membrane Proteins / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D018932:Chemokine CCL2 / Q000096:biosynthesis; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000096:biosynthesis; D054357:Chemokine CXCL10; D018925:Chemokines / Q000096:biosynthesis*; D019743:Chemokines, CXC / Q000096:biosynthesis; D005260:Female; D006801:Humans; D018950:Lipopolysaccharide Receptors; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis; D008297:Male; D009000:Monocytes / Q000378:metabolism; D016966:Porphyromonas gingivalis / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000378:metabolism*
D000942:Antigens, Bacterial; D018941:Antigens, CD19; D001425:Bacterial Outer Membrane Proteins; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D054357:Chemokine CXCL10; D018925:Chemokines; D019743:Chemokines, CXC; D018950:Lipopolysaccharide Receptors; D019402:Macrophage Inflammatory Proteins