title: Effects of oral commensal and pathogenic bacteria on human dendritic cells.
abstract: OBJECTIVE
  The oral cavity harbors a diverse and complex microbial community. Bacteria accumulate on both the hard and soft oral tissues in sessile biofilms and engage the host in an intricate cellular dialog, which normally constrains the bacteria to a state of commensal harmony. Dendritic cells (DCs) are likely to balance tolerance and active immunity to commensal microorganisms as part of chronic inflammatory responses. While the role played by DCs in maintaining intestinal homeostasis has been investigated extensively, relatively little is known about DC responses to oral bacteria.
  
  
  METHODS
  In this study, we pulsed human monocyte-derived immature DCs (iDCs) with cell wall extracts from pathogenic and commensal gram-positive or gram-negative oral bacteria.
  
  
  RESULTS
  Although all bacterial extracts tested induced iDCs to mature and produce cytokines/chemokines including interleukin-12p40, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 (MCP-1), the most important factor for programming DCs by oral bacteria was whether they were gram-positive or gram-negative, not whether they were commensal or pathogenic. In general, gram-negative oral bacteria, except for periodontopathic Porphyromonas gingivalis, stimulated DC maturation and cytokine production at lower concentrations than gram-positive oral bacteria. The threshold of bacteria needed to stimulate chemokine production was 100-fold to 1000-fold lower than that needed to induce cytokines. In addition, very low doses of oral commensal bacteria triggered monocytes to migrate toward DC-derived MCP-1.
  
  
  CONCLUSIONS
  Oral commensal and pathogenic bacteria do not differ qualitatively in how they program DCs. DC-derived MCP-1 induced in response to oral commensal bacteria may play a role, at least in part, in the maintenance of oral tissue integrity by attracting monocytes.
authors.affiliation: Department of Oral Biology, School of Dentistry, University of Washington, Seattle, WA 98195-7650, USA.
authors.forename: T
authors.initials: T
authors.lastname: Chino
authors.forename: D M
authors.initials: DM
authors.lastname: Santer
authors.forename: D
authors.initials: D
authors.lastname: Giordano
authors.forename: C
authors.initials: C
authors.lastname: Chen
authors.forename: C
authors.initials: C
authors.lastname: Li
authors.forename: C-H
authors.initials: CH
authors.lastname: Chen
authors.forename: R P
authors.initials: RP
authors.lastname: Darveau
authors.forename: E A
authors.initials: EA
authors.lastname: Clark
mesh_terms: D002473:Cell Wall / Q000737:chemistry; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis; D018925:Chemokines / Q000096:biosynthesis; D002634:Chemotaxis, Leukocyte; D016207:Cytokines / Q000096:biosynthesis; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D006090:Gram-Negative Bacteria / Q000502:physiology*; D006094:Gram-Positive Bacteria / Q000502:physiology*; D006801:Humans; D018928:Immunity, Mucosal / Q000502:physiology; D009000:Monocytes / Q000276:immunology; D009055:Mouth / Q000382:microbiology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D018932:Chemokine CCL2; D018925:Chemokines; D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha