| Co-Investigator(Kenkyū-buntansha) |
SHINOHARA Mitsuko Osaka Dental University, Dentistry, Associate Professor, 歯学部, 助教授 (40067187)
AZUMA Yasutaka Osaka Dental University, Dentistry, Assistant, 歯学部, 助手 (50298816)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2003: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
Macriphages are essential for controlling the majority of infections, and are mediators of natural immunity. During an infection, lipopolysaccharide (LPS) stimulates macrophages to produce proinflanimatory cytokines. Recently, it has been shown that A 2aadenosinereceptor (A2 aiR) is a critical part of the physiological negative feedback mechanism for the limitation and termination of tissue-specific and systemic inflammatory rsponseis It was useful and meaningful to gain information about interaction between LPS, which generates the inflammation, and adenosine receptors, which terminate the the inflamation. However, very little, if anything, is known about the effect of bacterial LPS on the expretion of A2aR during an infection of bacteria. The aim of this study is to evaluate the effect of adenosine,ATPand LPS on the espression of A2aR and LPS on the expression of A2aR and toll-like receptor 4(TLR4), which is a receptor for LPS, in the mouse macropharge cell line RAW 264. Adenosine and ATP failed to affect prolifaration in RAW 264 cells, whereas LPS increased proliferation. Adenosine significantly protentiated potentiated the expression of TLR4, hut not of A2aR ATP and LPS, markedly potentiated of the expression of A2aR and TLR4 in the presence of LPS, respenctively. Moreover adenosine and ATP did not affect the expression of A2aR and TLR 4 in the presences of LPS, respenctively. This study revealed that adenosine, ATP and LPS affect the exprettion of A2aR and TLR4 in macrophages.
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