title: Periodontal pathogens stimulate CC-chemokine production by mononuclear and bone-derived cells.
abstract: BACKGROUND
  Chemokines are chemotactic cytokines that stimulate recruitment of leukocytes. Monocyte chemoattractant protein-1, macrophage inflammatory protein-1alpha, and RANTES (regulated on activation, normal T cell expressed, and secreted) are 3 well-characterized CC-chemokines that regulate mononuclear cell recruitment. The recruitment of inflammatory cells is of particular importance in the oral cavity because of the likelihood that cells will be challenged with bacteria either during acute infection or following surgical procedures. Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans are putative periodontal pathogens that may be harbored in subgingival and supragingival plaque. The capacity of the host to respond to these bacteria by the elaboration of chemoattractants may represent an important defense mechanism.
  
  
  METHODS
  In the present study, we examined CC-chemokine production by human mononuclear cells and bone-derived cells in response to P. gingivalis, A. actinomycetemcomitans and lipopolysaccharides (LPS) stimulation in vitro. The chemokines produced were measured by ELISA.
  
  
  RESULTS
  The results demonstrate that P. gingivalis and A. actinomycetemcomitans induce high levels of MIP-1alpha in mononuclear cells. P. gingivalis and A. actinomycetemcomitans stimulated high levels of MCP-1 in bone-derived cells and induced moderate levels of RANTES production in both mononuclear and osteoblastic cells. In mononuclear cells, LPS induced high levels of MIP-1alpha and RANTES and moderate levels of MCP-1; in osteoblasts LPS only induced MCP-1.
  
  
  CONCLUSIONS
  The capacity of bacteria to induce a given chemokine depends upon the cell type stimulated. That different cell types would exhibit differences in the CC-chemokines produced under the same stimulus provides a mechanism to explain tissue-specific recruitment of leukocytes.
authors.affiliation: Department of Endodontics, Boston University School of Dental Medicine, MA, USA. yljiang@acs.bu.edu
authors.forename: Y
authors.initials: Y
authors.lastname: Jiang
authors.forename: D T
authors.initials: DT
authors.lastname: Graves
mesh_terms: D000328:Adult; D016976:Aggregatibacter actinomycetemcomitans / Q000276:immunology*; D000704:Analysis of Variance; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000096:biosynthesis; D019742:Chemokines, CC / Q000096:biosynthesis*; D002634:Chemotaxis, Leukocyte / Q000502:physiology; D003773:Dental Plaque / Q000382:microbiology; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D008070:Lipopolysaccharides / Q000276:immunology; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis; D009055:Mouth / Q000382:microbiology; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism*; D010006:Osteoblasts / Q000276:immunology / Q000378:metabolism*; D016966:Porphyromonas gingivalis / Q000276:immunology*
chemical_list: D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D019742:Chemokines, CC; D008070:Lipopolysaccharides; D019402:Macrophage Inflammatory Proteins