PMID- 11472436 OWN - NLM STAT- MEDLINE DCOM- 20010906 LR - 20220409 IS - 0009-9104 (Print) IS - 1365-2249 (Electronic) IS - 0009-9104 (Linking) VI - 125 IP - 1 DP - 2001 Jul TI - Chemokines in human periodontal disease tissues. PG - 134-41 AB - 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. FAU - Gemmell, E AU - Gemmell E AD - Immunopathology Laboratory, Oral Biology and Pathology, School of Dentistry, The University of Queensland, Brisbane, Australia. e.gemmell@mailbox.uq.edu.au FAU - Carter, C L AU - Carter CL FAU - Seymour, G J AU - Seymour GJ 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 (Chemokine CCL2) RN - 0 (Chemokine CCL4) RN - 0 (Chemokine CCL5) RN - 0 (Chemokine CXCL10) RN - 0 (Chemokines, CXC) RN - 0 (Macrophage Inflammatory Proteins) SB - IM MH - Chemokine CCL2/*biosynthesis MH - Chemokine CCL4 MH - Chemokine CCL5/*biosynthesis MH - Chemokine CXCL10 MH - Chemokines, CXC/*biosynthesis MH - Connective Tissue/immunology/pathology MH - Endothelium, Vascular/cytology/immunology MH - Gingiva/immunology/pathology MH - Humans MH - Keratinocytes/cytology/immunology MH - Macrophage Inflammatory Proteins/*biosynthesis MH - Periodontal Diseases/*immunology/pathology PMC - PMC1906105 EDAT- 2001/07/27 10:00 MHDA- 2001/09/08 10:01 PMCR- 2002/07/01 CRDT- 2001/07/27 10:00 PHST- 2001/07/27 10:00 [pubmed] PHST- 2001/09/08 10:01 [medline] PHST- 2001/07/27 10:00 [entrez] PHST- 2002/07/01 00:00 [pmc-release] AID - cei1511 [pii] AID - 10.1046/j.1365-2249.2001.01511.x [doi] PST - ppublish SO - Clin Exp Immunol. 2001 Jul;125(1):134-41. doi: 10.1046/j.1365-2249.2001.01511.x.