TY - JOUR
T1 - Increases in IL-33 production by fimbriae and lipopeptide from Porphyromonas gingivalis in mouse bone marrow-derived dendritic cells via toll-like receptor 2
AU - Tada, Hiroyuki
AU - Suzuki, Risako
AU - Nemoto, Eiji
AU - Shimauchi, Hidetoshi
AU - Matsushita, Kenji
AU - Takada, Haruhiko
N1 - Funding Information:
We thank D. Mrozek (Medical English Service) for English-language review of our paper. This work was supported by JSPS KAKENHI Grant Number 25463225 and the Takeda Science Foundation. The authors declare no potential conflicts of interest with respect to the authorship and/or publication of this article.
Publisher Copyright:
© 2017, Biomedical Research Foundation. All rights reserved.
PY - 2017
Y1 - 2017
N2 - 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 pathogenassociated 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.
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 pathogenassociated 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.
UR - http://www.scopus.com/inward/record.url?scp=85021157883&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85021157883&partnerID=8YFLogxK
U2 - 10.2220/biomedres.38.189
DO - 10.2220/biomedres.38.189
M3 - Article
C2 - 28637954
AN - SCOPUS:85021157883
SN - 0388-6107
VL - 38
SP - 189
EP - 195
JO - Biomedical Research
JF - Biomedical Research
IS - 3
ER -