Ansell Thomas K, Mitchell Howard W, McFawn Peter K, Noble Peter B
School of Veterinary and Life Sciences, Murdoch University, Murdoch.
School of Anatomy, Physiology and Human Biology, University of Western Australia, Crawley, Western Australia, Australia.
Respirology. 2016 Aug;21(6):1041-8. doi: 10.1111/resp.12800. Epub 2016 May 20.
While chronic inflammation of the airway wall and the failure of deep inspiration (DI) to produce bronchodilation are both common to asthma, whether pro-inflammatory cytokines modulate the airway smooth muscle response to strain during DI is unknown. The primary aim of the study was to determine how an inflammatory environment (simulated by the use of pro-inflammatory cytokines) alters the bronchodilatory response to DI.
We used whole porcine bronchial segments in vitro that were cultured in medium containing tumour necrosis factor and interleukin-1β for 2 days. A custom-built servo-controlled syringe pump and pressure transducer was used to measure airway narrowing and to simulate tidal breathing with intermittent DI manoeuvres.
Culture with tumour necrosis factor and interleukin-1β increased airway narrowing to acetylcholine but did not affect the bronchodilatory response to DI.
The failure of DI to produce bronchodilation in patients with asthma may not necessarily involve a direct effect of pro-inflammatory cytokines on airway tissue. A relationship between inflammation and airway hyper-responsiveness is supported, however, regulated by separate disease processes than those which attenuate or abolish the bronchodilatory response to DI in patients with asthma.
气道壁慢性炎症以及深吸气（DI）不能产生支气管舒张在哮喘中均很常见，但促炎细胞因子是否在DI期间调节气道平滑肌对牵张的反应尚不清楚。本研究的主要目的是确定炎症环境（通过使用促炎细胞因子模拟）如何改变对DI的支气管舒张反应。
我们在体外使用完整的猪支气管段，将其在含有肿瘤坏死因子和白细胞介素-1β的培养基中培养2天。使用定制的伺服控制注射泵和压力传感器来测量气道狭窄，并通过间歇性DI操作模拟潮式呼吸。
用肿瘤坏死因子和白细胞介素-1β培养会增加气道对乙酰胆碱的狭窄，但不影响对DI的支气管舒张反应。
哮喘患者中DI不能产生支气管舒张不一定涉及促炎细胞因子对气道组织的直接作用。然而，炎症与气道高反应性之间的关系得到支持，其受与哮喘患者中减弱或消除对DI的支气管舒张反应的疾病过程不同的独立疾病过程调节。
