PMID- 22984998
OWN - NLM
STAT- MEDLINE
DCOM- 20130402
LR  - 20151119
IS  - 1600-0722 (Electronic)
IS  - 0909-8836 (Linking)
VI  - 120
IP  - 5
DP  - 2012 Oct
TI  - Immunomodulation of dendritic cells differentiated in the presence of nicotine 
      with lipopolysaccharide from Porphyromonas gingivalis.
PG  - 408-14
LID - 10.1111/j.1600-0722.2012.00992.x [doi]
AB  - Tobacco smoking is a significant risk factor for periodontal diseases. Nicotine, 
      one of the most studied constituents in cigarette smoke, is thought to modify 
      immune responses. Dendritic cells (DCs), which are key mediators between innate 
      and adaptive immunity, stimulate naive T cells to differentiate to effector 
      T-cell subsets that may be actively involved in the immunopathogenesis of 
      periodontal diseases. In this study, we evaluated the effects of nicotine and 
      lipopolysaccharide (LPS) from Porphyromonas gingivalis, alone and in combination, 
      on the functions of human monocyte-derived DCs to elucidate the mechanism of 
      tissue destruction of smoking-associated periodontal diseases. P. gingivalis 
      LPS-stimulated DCs differentiated with nicotine (NiDCs) induced lower T-cell 
      proliferation and human leukocyte antigen (HLA)-DR expression, but elevated 
      expression of programmed cell death ligand 1. Additionally, NiDCs impaired 
      interferon-gamma production but maintained interleukin (IL)-5 and IL-10 production in 
      co-cultured T cells. Furthermore, NiDCs produced lower levels of proinflammatory 
      cytokines compared with DCs differentiated in the absence of nicotine. 
      Interestingly, NiDCs preferentially produced the T helper 2 (Th2)-type chemokines 
      macrophage chemotactic protein-1 and macrophage-derived chemokine. These results 
      suggest that the presence of nicotine during differentiation of DCs modulates the 
      immunoregulatory functions of P. gingivalis LPS-stimulated DCs.
CI  - (c) 2012 Eur J Oral Sci.
FAU - Yanagita, Manabu
AU  - Yanagita M
AD  - Department of Periodontology, Division of Oral Biology and Disease Control, Osaka 
      University Graduate School of Dentistry, Osaka, Japan.
FAU - Mori, Kenta
AU  - Mori K
FAU - Kobayashi, Ryohei
AU  - Kobayashi R
FAU - Kojima, Yuko
AU  - Kojima Y
FAU - Kubota, Mikiko
AU  - Kubota M
FAU - Miki, Koji
AU  - Miki K
FAU - Yamada, Satoru
AU  - Yamada S
FAU - Kitamura, Masahiro
AU  - Kitamura M
FAU - Murakami, Shinya
AU  - Murakami S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120828
PL  - England
TA  - Eur J Oral Sci
JT  - European journal of oral sciences
JID - 9504563
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharides)
RN  - 6M3C89ZY6R (Nicotine)
SB  - IM
MH  - Analysis of Variance
MH  - Cell Differentiation/drug effects/immunology
MH  - Cell Proliferation/drug effects
MH  - Cells, Cultured
MH  - Cytokines/*drug effects/metabolism
MH  - Dendritic Cells/*drug effects/immunology
MH  - Flow Cytometry
MH  - Humans
MH  - Lipopolysaccharides/*immunology/metabolism
MH  - Lymphocyte Activation/drug effects
MH  - Nicotine/metabolism/*pharmacology
MH  - Periodontal Diseases/*etiology/immunology
MH  - Porphyromonas gingivalis/*immunology/metabolism
MH  - T-Lymphocyte Subsets/*drug effects/metabolism
EDAT- 2012/09/19 06:00
MHDA- 2013/04/03 06:00
CRDT- 2012/09/19 06:00
PHST- 2012/07/01 00:00 [accepted]
PHST- 2012/09/19 06:00 [entrez]
PHST- 2012/09/19 06:00 [pubmed]
PHST- 2013/04/03 06:00 [medline]
AID - 10.1111/j.1600-0722.2012.00992.x [doi]
PST - ppublish
SO  - Eur J Oral Sci. 2012 Oct;120(5):408-14. doi: 10.1111/j.1600-0722.2012.00992.x. 
      Epub 2012 Aug 28.