2004 Fiscal Year Final Research Report Summary
Regulation of activation and cell death of neutrophils infiltrated into periapical lesions
| Project/Area Number |
15592029
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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 | MEIKAI UNIVERSITY |
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Principal Investigator |
TAKAHASHI Keiso Meikai University, School of Dentistry, Assistant Professor, 歯学部, 講師 (70243475)
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| Project Period (FY) |
2003 – 2004
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| Keywords | periapical lesion / oral PMNs / reactive oxygen species / signal transduction / antioxidants / apoptosis |
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| Research Abstract |
Although the cellular function and their physiology of peripheral neutrophils have been widely investigated, those of local neutrophils in oral cavity, intestine and mucosa have not well been known. It is crucial to investigate the mechanism by which regulates the cellular function of oral polymorphonuclear leukocytes (OPMN) in order to manipulate host defensive ability in the oral cavity. The aim of this study was to assess the status of cell activation and cell death of OPMN. OPMN were prepared by mouth rinse, filtration and Mono-Poly density gradient centrifugation method. Cellular activity of OPMN was assessed by superoxide production using NBT reagent. The cell death of OPMN was evaluated by flow cytometry using annexin V-FITC/propidium iodide staining. One to two millions OPMN was collected from each of healthy volunteers and 90% of freshly prepared OPMN were viable, as judged by trypan blue dye exclusion. OPMN produced significantly higher amounts of superoxide than peripheral PMN (p<0.05). The superoxide production by OPMN was significantly enhanced by PMA and Zymosan stimulation (p<0.05) and was not inhibited by H-7. OPMN died significantly faster at 37℃ than at 4℃ (p<0.05). Cell death of OPMN was partially inhibited by antioxidants, but was promoted by TNF-α. Caspase inhibitors and H-7 showed little effect. OPMN died via apoptosis and/or necrosis, and its ratio was varied by the types of stimulators. These results suggest that oral PMN are not activated via protein kinase C and that oxidative stress enhances apoptosis of OPMN. Further research will be required to investigate the underlying mechanism relating with cell activation and cell death of OPMN.
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