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Ozone-induced airway hyperresponsiveness: roles of ROCK isoforms

机译：臭氧诱导的气道高反应性：岩石同种型的角色

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摘要

Acute ozone (O_3) inhalation has been shown to cause airway and pulmonary epithelial injury with accompanying inflammation responses. Robust evidence exists that O_3 induces airway hyperresponsiveness (AHR) in humans and in animal models. Several pathways exist that culminate in airway smooth muscle contraction, but the mechanism(s) by which O_3 elicits AHR are unclear. Here, we review the recent report by Kasahara et al. (Kasahara DI, Mathews JA, Park CY, Cho Y, Hunt G, Wurmbrand AP, Liao JK, Shore SA. Am J Physiol Lung Cell Mol Physiol 309: L736-L746) describing the role of two Rho kinase (ROCK) isoforms in О3-induced AHR utilizing a murine haploinsufficiency model. Compared with wild-type (WT) mice, the authors report that ROCK1~(+/-) and ROCK2~(+/-) mice exhibited significantly reduced AHR following acute exposure to O_3. Additionally, WT mice treated with fasudil, an FDA-approved ROCK1/2 inhibitor, recapitulated reduction in AHR as seen in ROCK haplotypes. It was suggested that, although the two ROCK isoforms are both induced by Rho, they have different mechanisms by which they mediate О_3-induced AHR: ROCK1 via hyaluronan signaling vs. ROCK2 acting downstream of inflammation at the level of airway smooth muscle contraction. These observations provide an important framework to develop novel ROCK-targeting therapies for acute О_3-induced AHR.
机译：已经显示急性臭氧（O_3）吸入导致气道和肺上皮损伤与随附的炎症反应。有稳健的证据表明O_3诱导人类和动物模型中的气道高反应性（AHR）。存在几种途径，达到气道平滑肌收缩，但是o_3引发AHR的机制尚不清楚。在这里，我们审查了Kasahara等人的最近报告。 （Kasahara di，Mathews Ja，Park Cy，Cho Y，Hunt G，Wurmbrand AP，Liao JK，Shore SA。AM J Physiol肺细胞Mol Physiol 309：L736-L746）描述两种Rho激酶（岩石）同种型的作用О3诱导的AHR利用小鼠淘水能机构模型。与野生型（WT）小鼠相比，作者报告称Rock1〜（+/-）和Rock2〜（+/-）小鼠在急性暴露于O_3之后显着降低了AHR。另外，用Fasudil处理的WT小鼠，FDA批准的ROCK1 / 2抑制剂，如岩石单倍型所示的AHR综合减少。有人建议，虽然两种岩石同种型都是由rho诱导的，但它们具有不同的机制，通过其介导静电诱导的AHR：Rock1通过透明质酸的信号与岩体在气道平滑肌肉收缩水平下作用下游。这些观察结果提供了一种为急性®3诱导的AHR开发新型岩靶疗法的重要框架。

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