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首页> 外文期刊>American Journal of Physiology >Role of CD38 in TNF-a-induced airway hyperresponsiveness
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Role of CD38 in TNF-a-induced airway hyperresponsiveness

机译：CD38在TNF-a诱导的气道高反应性中的作用

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First published November 30, 2007; doi:10.1152/ajplung.00367.2007.-CD38 is involved in normal airway function, IL~(-1)3-induced airway hyperresponsiveness (AHR), and is also regulated by tumor necrosis factor (TNF)-alpha: in airway smooth muscle (ASM) cells. This study aimed to determine whether TNF-a-induced CD38 upregulation in ASM cells contributes to AHR, a hallmark of asthma. We hypothesized that AHR would be attenuated in TNF-a-exposed CD38-deficient (CD38KO) mice compared with wild-type (WT) controls. Mice (n - 6-8/group) were intranasally challenged with vehicle control or TNF-alpha (50 ng) once and every other day during 1 or 4 wk. Lung inflammation and AHR, measured by changes in lung resistance after inhaled metha-choline, were assessed 24 h following the last challenge. Tracheal rings were incubated with TNF-alpha (50 ng/ml) to assess contractile changes in the ASM. While a single TNF-alpha challenge caused no airway inflammation, both multiple-challenge protocols induced equally significant inflammation in CD38KO and WT mice. A single intranasal TNF-alpha challenge induced AHR in the WT but not in the CD38KO mice, whereas both mice developed AHR after 1 wk of challenges. The AHR was suppressed by extending the challenges for 4 wk in both mice, although to a larger magnitude in the WT than in the CD38KO mice. TNF-alpha increased ASM contractile properties in tracheal rings from WT but not from CD38KO mice. In conclusion, CD38 contributes to TNF-a-induced AHR after a brief airway exposure to the cytokine, likely by mediating changes in ASM contractile responses, and is associated with greater AHR remission following chronic airway exposure to TNF-alpha. The mechanisms involved in this remission remain to be determined.
机译：首次发布于2007年11月30日; doi：10.1152 / ajplung.00367.2007.-CD38参与正常的气道功能，IL〜（-1）3-诱导的气道高反应性（AHR），并且还受肿瘤坏死因子（TNF）-alpha的调节：在气道平滑肌中（ASM）单元。这项研究旨在确定TNF-α诱导的ASM细胞CD38上调是否有助于AHR（哮喘的标志）。我们假设与野生型（WT）对照相比，TNF-α暴露的CD38缺陷（CD38KO）小鼠中AHR会减弱。在1或4周内，每隔一天一次对小鼠（n-6-8 /组）进行鼻内媒介物对照或TNF-alpha（50 ng）攻击。在最后一次攻击后24小时，通过吸入乙酰甲胆碱后肺阻力的变化来测量肺部炎症和AHR。将气管环与TNF-α（50 ng / ml）孵育以评估ASM中的收缩变化。尽管单个TNF-α攻击未引起气道炎症，但两种多攻击方案均在CD38KO和WT小鼠中诱导了同样显着的炎症。单个鼻内TNF-α攻击在WT中诱导了AHR，但在CD38KO小鼠中却没有，但两只小鼠在攻击1周后都产生了AHR。尽管在WT中比在CD38KO小鼠中具有更大的强度，但是通过在两只小鼠中将挑战延长4周来抑制了AHR。 TNF-α增加了WT的气管环中ASM的收缩特性，但没有增加CD38KO小鼠的气管环中的ASM收缩特性。总之，CD38在短暂的气道暴露于细胞因子后，可能通过介导ASM收缩反应的变化而促成TNF-α诱导的AHR，并与慢性气道暴露于TNF-α后的更大的AHR缓解相关。缓解的机制尚待确定。

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