PMID- 19239635
OWN - NLM
STAT- MEDLINE
DCOM- 20090616
LR  - 20211020
IS  - 1399-302X (Electronic)
IS  - 0902-0055 (Print)
IS  - 0902-0055 (Linking)
VI  - 24
IP  - 2
DP  - 2009 Apr
TI  - Effects of oral commensal and pathogenic bacteria on human dendritic cells.
PG  - 96-103
LID - 10.1111/j.1399-302X.2008.00478.x [doi]
AB  - BACKGROUND/AIMS: 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. CONCLUSION: 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.
FAU - Chino, T
AU  - Chino T
AD  - Department of Oral Biology, School of Dentistry, University of Washington, 
      Seattle, WA 98195-7650, USA.
FAU - Santer, D M
AU  - Santer DM
FAU - Giordano, D
AU  - Giordano D
FAU - Chen, C
AU  - Chen C
FAU - Li, C
AU  - Li C
FAU - Chen, C-H
AU  - Chen CH
FAU - Darveau, R P
AU  - Darveau RP
FAU - Clark, E A
AU  - Clark EA
LA  - eng
GR  - R01 DE016381/DE/NIDCR NIH HHS/United States
GR  - AI44257/AI/NIAID NIH HHS/United States
GR  - DE16381/DE/NIDCR NIH HHS/United States
GR  - R01 AI044257/AI/NIAID NIH HHS/United States
GR  - R37 AI044257/AI/NIAID NIH HHS/United States
GR  - R01 DE016381-04/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - Denmark
TA  - Oral Microbiol Immunol
JT  - Oral microbiology and immunology
JID - 8707451
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Tumor Necrosis Factor-alpha)
MH  - Cell Wall/chemistry
MH  - Cells, Cultured
MH  - Chemokine CCL2/biosynthesis
MH  - Chemokines/biosynthesis
MH  - Chemotaxis, Leukocyte
MH  - Cytokines/biosynthesis
MH  - Dendritic Cells/immunology/metabolism/*microbiology
MH  - Gram-Negative Bacteria/*physiology
MH  - Gram-Positive Bacteria/*physiology
MH  - Humans
MH  - Immunity, Mucosal/physiology
MH  - Monocytes/immunology
MH  - Mouth/*microbiology
MH  - Tumor Necrosis Factor-alpha/biosynthesis
PMC - PMC2733846
MID - NIHMS122163
EDAT- 2009/02/26 09:00
MHDA- 2009/06/17 09:00
PMCR- 2010/04/01
CRDT- 2009/02/26 09:00
PHST- 2009/02/26 09:00 [entrez]
PHST- 2009/02/26 09:00 [pubmed]
PHST- 2009/06/17 09:00 [medline]
PHST- 2010/04/01 00:00 [pmc-release]
AID - OMI478 [pii]
AID - 10.1111/j.1399-302X.2008.00478.x [doi]
PST - ppublish
SO  - Oral Microbiol Immunol. 2009 Apr;24(2):96-103. doi: 
      10.1111/j.1399-302X.2008.00478.x.