2005 Fiscal Year Final Research Report Summary
Analysis of the role of pulp fibroblasts on lymphocytes infiltration in pulpitis
| Project/Area Number |
16591915
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Conservative dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
FUJINAKA Keiko The University of Tokushima, University Medical and Dental Hospital, Research Associate, 医学部・歯学部附属病院, 助手 (00294710)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAE Hideaki The University of Tokushima, Institute of Health Biosciences, Assistant Professor, 大学院・ヘルスバイオサイエンス研究部, 助教授 (30227730)
OZAKI Kazumi The University of Tokushima, University Medical and Dental Hospital, Lecturer, 医学部・歯学部附属病院, 講師 (90214121)
HOSOKAWA Yoshitaka The University of Tokushima, University Medical and Dental Hospital, Research Associate, 医学部・歯学部附属病院, 助手 (90346601)
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| Project Period (FY) |
2004 – 2005
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| Keywords | pulpitis / chemokine / cytokine / bacteria-related products / fibroblast / periodontal disease |
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| Research Abstract |
Pulpitis resulting from dental caries is characterized by marked inflammatory cells such as lymphocytes. Periodontal disease is also characterized as chronic inflammation associated with Gram-negative bacteria in the oral cavity, and many inflammatory cells are infiltrated in periodontally diseased tissues. However, little is known about the mechanism of inflammatory cells recruitment into the inflammatory regions. In this study, we focused on chemokines that are related to inflammatory cells infiltration. We investigated chemokine expression in pulpitis tissues and periodontally diseased tissues. Furthermore, we examined the capability of pulp fibroblasts and gingival fibroblasts for chemokine production.
We detected CCL20 and CXCL10 that are involved in T cell infiltration in pulpitis tissues, and we also detected CCR6 (CCL20 receptor) and CXCR3 (CXCL10 receptor) positive inflammatory cells in pulpitis tissues. In periodontally diseased tissues, we detected CCL20, CXCL12 and fractalkine that are also related to lymphocyte infiltration in periodontally diseased tissues, and we also detected CCR6, CXCR4 (CXCL12 receptor) and CX3CR1 (fractalkine receptor) positive cells infiltration in periodontally diseased tissues. Moreover, we revealed that CXCL10 production by pulp fibroblasts was up-regulated by proinflammatory cytokines (TNF-α and IFN-γ) and E.coli LPS. Furthermore, we elucidated CCL20 and CXCL12 production was enhanced by proinflammatory cytokines (IL-1β, TNF-α and IFN-γ) and bacteria-related products (E.coli LPS, S.aureus LTA, CpG DNA) stimulation.
These results show that fibroblasts in pulp tissues and periodontal tissues can control inflammatory cells infiltration because these cells can produce chemokines by cytokine or bacteria stimulation. It is known that inflammatory cells in inflammatory region are involved in the progress of pulpitis and periodontal disease. So, chemokine will be a target for pulpitis and periodontal disease therapy.
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