| Project/Area Number |
15590818
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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 |
Respiratory organ internal medicine
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| Research Institution | Oita University (2004)
大分医科大学 (2003) |
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Principal Investigator |
MIYAZAKI Eishi Oita University, Faculty of Medicine, Department of Internal Medicine, Associate Professor, 医学部, 助教授 (00264333)
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| Co-Investigator(Kenkyū-buntansha) |
ANDO Masaru Oita University, Faculty of Medicine, Department of Internal Medicine, Instructor, 医学部, 助手 (20336267)
FUKAMI Tetsujiro Oita University, Faculty of Medicine, Department of Internal Medicine, Instructor, 医学部, 助手 (30363568)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2003: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | acute eosinophilic pneumonia / cigarette smoke / TARC / MDC / dendritic cell / alveolar macrophage / 気管支肺胞洗浄 / チャレンジテスト |
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| Research Abstract |
Acute eosinophilic pneumonia(AEP) is characterized by an acute febrile illness with severe hypoxemia, diffuse pulmonary infiltrates, and an increase in bronchoalveolar lavage(BAL) eosinophils. AEP may be a common pathway of lung inflammation in response to a variety of possible antigens, including cigarette smoke. CC chemokines such as thymus- and activation-regulated chemokine(TARC/CCL17) and macrophage-derived chemokine(MDC/CCL21), which are functional ligands for CCR4, have been reported to be expressed in various allergic diseases such as atopic dermatitis, bronchial asthma and eosinophilic pneumonia. We examined the production of MDC and TARC by bronchoalveolar lavage fluid(BALF) cells in cigarette-smoke-associated acute eosinophilic pneumonia(CS-AEP). The CC chemokine Receptor-4(CCR4) ligand levels in BALF from patients with CS-AEP were considerably higher than those in healthy volunteers and correlated well with Th2 cytokine levels, such as interleukin(IL)-4, IL-5 and IL-13. IL-4, but not tumor necrosis factor-alpha, interferon-gamma or LPS, enhanced CCR4 ligand production by BALF cells. By immunocytochemistry, MDC expression was observed in CD68-positive cells from patients with CS-AEP and in healthy control smokers. In contrast, TARC expression in CD68- or CD1a-positive cells was detected only in CS-AEP. An in vivo cigarette smoke challenge test induced increases in CCR4 ligands in the BALF and in the cultured supernatant of BALF adherent cells. These results suggest that alveolar macrophages and dendritic cells contribute to the pathogenesis of CS-AEP by generating CCR4 ligands, probably in response to cigarette smoke.
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