Interactions between airway smooth murle cells and inflammatory cells in the pathogenesis of asthma

哮喘发病机制中气道平滑肌细胞与炎症细胞的相互作用

基本信息

项目摘要

It has been suggested that airway smooth muscle cells play important roles in the pathogenesis of asthma, but precise mechanisms remain unclear W efocused on the interactions between these structural cells and inflammatory cells such as T cells, mast cells and eosinophils Human airway smooth muscle cells express and release stem cell factor, TGF beat family molecules and and versican. These factors are believed to be chemotactic for mast cells and also be involved in airway wall remodling.IL-9, a class of Th2 type cytokine, is a potent inducer acting on airway smooth muscle cells.Airway structural cells are once believed to be terminally differentiated cells, but recent reports strongly suggest that even these cells may change in to other type of cells. We demonstrated that human epithelial cells showed a distinct epithelial mesenchymal transition (EMT) upon stimulation of TGFbeta. These changes were induced by TNFalpha. It was suggested that dynamic interactions between airway structural cells and inflammatory cells via cytokines and growth factors play important roles in the regulation of airway remodeling in the pathogenesis of asthma. These new finding may highlight a way to develop novel type of anti-asthma drugs preventing remodeling, an irreversible airway change
气道平滑肌细胞在哮喘的发病机制中起重要作用,但其确切机制尚不清楚,我们主要研究这些结构细胞与T细胞、肥大细胞和嗜酸性粒细胞等炎症细胞的相互作用。IL-9是一类Th 2型细胞因子,是一种作用于气道平滑肌细胞的强诱导因子,气道结构细胞曾被认为是终末分化细胞,但最近的研究表明,这些细胞也可能向其他类型的细胞转化。我们证明,人类上皮细胞显示出一个独特的上皮间质转化(EMT)刺激TGF β。这些变化由TNF α诱导。提示气道结构细胞与炎症细胞通过细胞因子和生长因子的动态相互作用在哮喘气道重塑的调控中起重要作用。这些新发现可能为开发新型抗哮喘药物提供了一种方法,可以防止气道重塑,这是一种不可逆的气道变化

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Methotrexate induces proinflammatory cytokines production by human bronchial and alveolar epithelial cells
甲氨蝶呤诱导人支气管和肺泡上皮细胞产生促炎细胞因子
  • DOI:
  • 发表时间:
    2006
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Yamauchi Y;et. al.
  • 通讯作者:
    et. al.
Airway inflammatory responses to oxidative stress induced by prolonged low-dose diesel exhaust particle exposure from birth differ between mouse BALB/C and C57BL/6 strains
  • DOI:
    10.1080/01902140701884406
  • 发表时间:
    2008-03-01
  • 期刊:
  • 影响因子:
    1.7
  • 作者:
    Li, Ying-Ji;Kawada, Tomoyuki;Kohyama, Tadashi
  • 通讯作者:
    Kohyama, Tadashi
TGF-beta1 and serum both stimulate contraction but differentially affect apoptosis in 3D collagen gels.
TGF-β1 和血清均刺激收缩,但对 3D 胶原凝胶中的细胞凋亡影响不同。
  • DOI:
  • 发表时间:
    2006
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Matsumoto;A.;Hiramatsu;K.;Li;Y.;Azuma;A.;Kudoh;S.;Takizawa;H.;Sugawara;I;Kobayashi T et al.;Fang Q et al.;幸山 正;Kobayashi T et al.
  • 通讯作者:
    Kobayashi T et al.
Repeated exposure to low-dose diesel exhaust after allergen challenge exaggerates asthmatic responses in mice
  • DOI:
    10.1016/j.clim.2006.08.003
  • 发表时间:
    2006-11-01
  • 期刊:
  • 影响因子:
    8.6
  • 作者:
    Matsumoto, Aki;Hiramatsu, Kumiko;Sugawara, Isamu
  • 通讯作者:
    Sugawara, Isamu
Novel strategies for the treatment of asthma.
  • DOI:
    10.1007/s40629-016-0093-5
  • 发表时间:
    2016
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Lommatzsch M;Stoll P
  • 通讯作者:
    Stoll P
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TAKIZAWA Hajime其他文献

TAKIZAWA Hajime的其他文献

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{{ truncateString('TAKIZAWA Hajime', 18)}}的其他基金

Interactions of myofibroblasts with airway epithelial cells in allergic airway inflammation
过敏性气道炎症中肌成纤维细胞与气道上皮细胞的相互作用
  • 批准号:
    14570543
  • 财政年份:
    2002
  • 资助金额:
    $ 10.5万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Molecular mechanisms of chemokine gene expression in allergic airway inflammation : Selective induction of eotaxin and TARC by Th2 cytokines in airway epithelial cells
过敏性气道炎症趋化因子基因表达的分子机制:气道上皮细胞中Th2细胞因子选择性诱导eotaxin和TARC
  • 批准号:
    12670551
  • 财政年份:
    2000
  • 资助金额:
    $ 10.5万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Role of airway epithelial cells in the accumulation and activation of T cells in allergic airway inflammation
气道上皮细胞在过敏性气道炎症中 T 细胞积累和激活中的作用
  • 批准号:
    10670533
  • 财政年份:
    1998
  • 资助金额:
    $ 10.5万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
気管支喘息の気道傷害後の修復とリモデリングにおける成長因子の役割-特にトランスフォーミング成長因子β(TGFβ)を中心に-
生长因子在支气管哮喘气道损伤后修复和重塑中的作用 - 特别关注转化生长因子 β (TGFβ) -
  • 批准号:
    08670656
  • 财政年份:
    1996
  • 资助金额:
    $ 10.5万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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RUI:仿生微环境中集体细胞迁移的机械调节
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    2342274
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    2339054
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揭示定向细胞迁移的潜在生物物理机制
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    2345411
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    2024
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    $ 10.5万
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    Standard Grant
Collaborative Research: DMS/NIGMS 1: Simulating cell migration with a multi-scale 3D model fed by intracellular tension sensing measurements
合作研究:DMS/NIGMS 1:使用由细胞内张力传感测量提供的多尺度 3D 模型模拟细胞迁移
  • 批准号:
    2347957
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    2024
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    $ 10.5万
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Collaborative Research: DMS/NIGMS 1: Simulating cell migration with a multi-scale 3D model fed by intracellular tension sensing measurements
合作研究:DMS/NIGMS 1:使用由细胞内张力传感测量提供的多尺度 3D 模型模拟细胞迁移
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线粒体定位调节细胞迁移过程中的氧化还原信号
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    10520211
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细胞迁移中 Rho GTP 酶之间串扰的肌动蛋白门控
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