<b>Increases in IL-33 production by fimbriae and lipopeptide from </b><i><b>Porphyromonas gingivalis</b></i><b> in mouse bone marrow-derived dendritic cells via Toll-like receptor </b><b>2 </b>
-
- TADA Hiroyuki
- Division of Oral Microbiology, Tohoku University Graduate School of Dentistry
-
- SUZUKI Risako
- Division of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
-
- NEMOTO Eiji
- Division of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
-
- SHIMAUCHI Hidetoshi
- Division of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
-
- MATSUSHITA Kenji
- Department of Oral Disease Research, National Center for Geriatrics and Gerontology
-
- TAKADA Haruhiko
- Division of Oral Microbiology, Tohoku University Graduate School of Dentistry
Search this article
Abstract
<p>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.</p>
Journal
-
- Biomedical Research
-
Biomedical Research 38 (3), 189-195, 2017
Biomedical Research Press