Chemokines in human periodontal disease tissues.
An immunoperoxidase technique was used to examine IP-10 (interferon-gamma inducible protein 10), RANTES (regulated on activation normal T cell expressed and secreted), MCP-1 (monocyte chemoattractant protein-1), and MIP-1 alpha (macrophage inflammatory protein-1 alpha) in gingival biopsies from 21 healthy/gingivitis and 26 periodontitis subjects. The samples were placed into 3 groups according to the size of infiltrate. MIP-1 alpha+ cells were more abundant than the other chemokines with few MCP-1+ cells. The mean percent MIP-1 alpha+ cells was higher than the percent MCP-1+ cells (P = 0.02) in group 2 (intermediate size infiltrates) lesions from periodontitis subjects, other differences not being significant due to the large variations between tissue samples. Analysis of positive cells in relation to CD4/CD8 ratios showed that with an increased proportion of CD8+ cells, the mean percent MIP-1 alpha+ cells was significantly higher in comparison with the mean percent RANTES+ and MCP-1+ cells (P < 0.015). Endothelial cells were MCP-1+ although positive capillaries were found on the periphery of infiltrates only. Keratinocyte expression of chemokines was weak and while the numbers of healthy/gingivitis and periodontitis tissue sections positive for IP-10, RANTES and MCP-1 reduced with increasing inflammation, those positive for MIP-1 alpha remained constant for all groups. In conclusion, fewer leucocytes expressed MCP-1 in gingival tissue sections, however, the percent MIP-1 alpha+ cells was increased particularly in tissues with increased proportions of CD8 cells and B cells with increasing inflammation and also in tissues with higher numbers of macrophages with little inflammation. Further studies are required to determine the significance of MIP-1 alpha in periodontal disease.
Gemmell
E
E
Immunopathology Laboratory, Oral Biology and Pathology, School of Dentistry, The University of Queensland, Brisbane, Australia. e.gemmell@mailbox.uq.edu.au
Carter
C L
CL
Seymour
G J
GJ
D018932:Chemokine CCL2 / Q000096:biosynthesis*; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000096:biosynthesis*; D054357:Chemokine CXCL10; D019743:Chemokines, CXC / Q000096:biosynthesis*; D003238:Connective Tissue / Q000276:immunology / Q000473:pathology; D004730:Endothelium, Vascular / Q000166:cytology / Q000276:immunology; D005881:Gingiva / Q000276:immunology / Q000473:pathology; D006801:Humans; D015603:Keratinocytes / Q000166:cytology / Q000276:immunology; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis*; D010510:Periodontal Diseases / Q000276:immunology* / Q000473:pathology
D018932:Chemokine CCL2; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D054357:Chemokine CXCL10; D019743:Chemokines, CXC; D019402:Macrophage Inflammatory Proteins