• 我要登录|
  • 免费注册
    |
  • 我的丁香通
    • 企业机构:
    • 成为企业机构
    • 个人用户:
    • 个人中心
  • 移动端
    移动端
丁香通 logo丁香实验_LOGO
搜实验

    大家都在搜

      大家都在搜

        0 人通过求购买到了急需的产品
        免费发布求购
        发布求购
        点赞
        收藏
        wx-share
        分享

        Current In Vitro Models of Leukocyte Migration: Methods and Interpretation

        互联网

        310
        A large component of airway inflammatory disease is the recruitment of activated leukocytes (primarily eosinophils and T lymphocytes) from the lung vasculature into the bronchial walls resulting in lung edema. Ultimately, many of the infiltrating leukocytes progress across the airway epithelium into respiratory bronchioles, compromising lung capacity (1 ,2 ). In the case of an infection, such as pneumonia, leukocytes (primarily neutrophils and monocyte/macrophages) are recruited to alveolar air spaces reducing the capacity for gaseous exchange. In both cases, resident leukocytes then release further factors that promote additional leukocyte recruitment. During an inflammatory response in the peripheral microvasculature leukocyte recruitment takes place predominantly in the postcapillary venules via the multistep adhesion cascade (reviewed in 3 ,4 ,5 ). In the lung, however, leukocyte extravasation takes place via capillaries. This may be due to the specialized architecture of the lung vasculature (e.g., large numbers of branch points), or because of the differing expression of surface adhesion molecules that are required for leukocyte recruitment (1 ,6 ). In addition, local concentrations of cytokines, chemokines or other chemoattractant factors will play a role in the site and degree of leukocyte infiltration (7 ,8 ) through acute local activation of endothelial cells.
        ad image
        提问
        扫一扫
        丁香实验小程序二维码
        实验小助手
        丁香实验公众号二维码
        扫码领资料
        反馈
        TOP
        打开小程序