PMID- 28637954
OWN - NLM
STAT- MEDLINE
DCOM- 20180326
LR  - 20180326
IS  - 1880-313X (Electronic)
IS  - 0388-6107 (Linking)
VI  - 38
IP  - 3
DP  - 2017
TI  - Increases in IL-33 production by fimbriae and lipopeptide from Porphyromonas 
      gingivalis in mouse bone marrow-derived dendritic cells via Toll-like receptor 2.
PG  - 189-195
LID - 10.2220/biomedres.38.189 [doi]
AB  - Interleukin-33 (IL-33) is an IL-1 cytokine family member that is involved in the 
      development of chronic inflammatory diseases and the initiation of allergic 
      inflammation in response to pathogens. Porphyromonas gingivalis is a primary 
      pathogen that is involved in chronic periodontitis and its bacterial components 
      induce inflammatory responses. Dendritic cells (DCs) recognize pathogen- 
      associated molecular patterns by expression of pattern-recognition receptors, 
      such as Toll-like receptors (TLRs). DCs play an essential role in resistance to 
      infection and maintenance of mucosal immune system. In this study, we 
      investigated whether P. gingivalis increases the expression of IL-33 in mouse 
      bone marrow-derived DCs (BMDCs). BMDCs exhibited an increased expression of IL-33 
      mRNA upon stimulation with P. gingivalis whole cells. Furthermore, fimbriae and 
      lipopeptide derived from P. gingivalis exhibited higher IL-33 mRNA expression 
      than P. gingivalis whole cells. In contrast, lipopolysaccharide derived from P. 
      gingivalis did not induce IL-33 mRNA expression in BMDCs. The IL-33 mRNA 
      expression after stimulation with fimbriae or lipopeptide was up-regulated in 
      BMDCs from wild-type mice but not from TLR2-deficient (TLR2(-/-)) mice. IL-33 
      production induced by fimbriae and lipopeptide accumulated in the cytoplasm of 
      BMDCs from wild-type mice, but not from TLR2(-/-) mice. These findings suggested 
      that IL-33 production induced by P. gingivalis fimbriae and lipopeptide is 
      recognized by TLR2 and may modulate DC function in periodontal diseases.
FAU - Tada, Hiroyuki
AU  - Tada H
AD  - Division of Oral Microbiology, Tohoku University Graduate School of Dentistry.
FAU - Suzuki, Risako
AU  - Suzuki R
AD  - Division of Periodontology and Endodontology, Tohoku University Graduate School 
      of Dentistry.
FAU - Nemoto, Eiji
AU  - Nemoto E
AD  - Division of Periodontology and Endodontology, Tohoku University Graduate School 
      of Dentistry.
FAU - Shimauchi, Hidetoshi
AU  - Shimauchi H
AD  - Division of Periodontology and Endodontology, Tohoku University Graduate School 
      of Dentistry.
FAU - Matsushita, Kenji
AU  - Matsushita K
AD  - Department of Oral Disease Research, National Center for Geriatrics and 
      Gerontology.
FAU - Takada, Haruhiko
AU  - Takada H
AD  - Division of Oral Microbiology, Tohoku University Graduate School of Dentistry.
LA  - eng
PT  - Journal Article
PL  - Japan
TA  - Biomed Res
JT  - Biomedical research (Tokyo, Japan)
JID - 8100317
RN  - 0 (Il33 protein, mouse)
RN  - 0 (Interleukin-33)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tlr2 protein, mouse)
RN  - 0 (Tlr4 protein, mouse)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (Toll-Like Receptor 4)
SB  - IM
MH  - Animals
MH  - Bacteroidaceae Infections/*immunology/metabolism/microbiology
MH  - Bone Marrow/pathology
MH  - Cells, Cultured
MH  - Dendritic Cells/immunology/*metabolism/microbiology
MH  - Fimbriae, Bacterial/immunology
MH  - Gene Expression
MH  - Gingivitis/*immunology/metabolism/microbiology
MH  - Interleukin-33/*biosynthesis/genetics
MH  - Lipopolysaccharides/pharmacology
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Porphyromonas gingivalis/*immunology
MH  - Toll-Like Receptor 2/genetics/*metabolism
MH  - Toll-Like Receptor 4/metabolism
MH  - Transcriptional Activation
EDAT- 2017/06/24 06:00
MHDA- 2018/03/27 06:00
CRDT- 2017/06/23 06:00
PHST- 2017/06/23 06:00 [entrez]
PHST- 2017/06/24 06:00 [pubmed]
PHST- 2018/03/27 06:00 [medline]
AID - 10.2220/biomedres.38.189 [doi]
PST - ppublish
SO  - Biomed Res. 2017;38(3):189-195. doi: 10.2220/biomedres.38.189.