Centre for Asthma and Respiratory Disease and Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia.
Thorax. 2015 May;70(5):458-67. doi: 10.1136/thoraxjnl-2014-206067. Epub 2015 Mar 6.
Steroid-insensitive endotypes of asthma are an important clinical problem and effective therapies are required. They are associated with bacterial infection and non-eosinophilic inflammatory responses in the asthmatic lung. Macrolide therapy is effective in steroid-insensitive endotypes, such as non-eosinophilic asthma. However, whether the effects of macrolides are due to antimicrobial or anti-inflammatory mechanisms is not known.
To determine and assess the efficacy of macrolide (ie, clarithromycin) and non-macrolide (ie, amoxicillin) antibiotic treatments in experimental models of infection-induced, severe, steroid-insensitive neutrophilic allergic airways disease (SSIAAD), compared with steroid-sensitive AAD and to delineate the antimicrobial and anti-inflammatory effects of macrolide therapy.
We developed and used novel mouse models of Chlamydia and Haemophilus lung infection-induced SSIAAD. We used these models to investigate the effects of clarithromycin and amoxicillin treatment on immune responses and airways hyper-responsiveness (AHR) in Ova-induced, T helper lymphocyte (Th) 2 -associated steroid-sensitive AAD and infection-induced Th1/Th17-associated SSIAAD compared with dexamethasone treatment.
Clarithromycin and amoxicillin had similar antimicrobial effects on infection. Amoxicillin did attenuate some features, but did not broadly suppress either form of AAD. It did restore steroid sensitivity in SSIAAD by reducing infection. In contrast, clarithromycin alone widely suppressed inflammation and AHR in both steroid-sensitive AAD and SSIAAD. This occurred through reductions in Th2 responses that drive steroid-sensitive eosinophilic AAD and tumour necrosis factor α and interleukin 17 responses that induce SSIAAD.
Macrolides have broad anti-inflammatory effects in AAD that are likely independent of their antimicrobial effects. The specific responses that are suppressed are dependent upon the responses that dominate during AAD.
哮喘的类固醇不敏感表型是一个重要的临床问题,需要有效的治疗方法。它们与哮喘肺部的细菌感染和非嗜酸性炎症反应有关。大环内酯类治疗对类固醇不敏感表型如非嗜酸性哮喘有效。然而,大环内酯类的作用是由于抗菌还是抗炎机制尚不清楚。
在感染诱导的严重、类固醇不敏感的中性粒细胞性过敏性气道疾病(SSIAAD)的实验模型中,确定和评估大环内酯类(即克拉霉素)和非大环内酯类(即阿莫西林)抗生素治疗的疗效,与类固醇敏感的 AAD 进行比较,并阐明大环内酯类治疗的抗菌和抗炎作用。
我们开发并使用了新型的衣原体和嗜血杆菌肺部感染诱导的 SSIAAD 小鼠模型。我们使用这些模型来研究克拉霉素和阿莫西林治疗对卵清蛋白诱导的 Th2 相关类固醇敏感的 AAD 和感染诱导的 Th1/Th17 相关 SSIAAD 中免疫反应和气道高反应性(AHR)的影响,并与地塞米松治疗进行比较。
克拉霉素和阿莫西林对感染具有相似的抗菌作用。阿莫西林虽然可以减轻某些特征,但不能广泛抑制任何一种 AAD。它通过减少感染来恢复 SSIAAD 的类固醇敏感性。相比之下,克拉霉素单独广泛抑制了类固醇敏感的 AAD 和 SSIAAD 中的炎症和 AHR。这是通过减少驱动类固醇敏感嗜酸性 AAD 的 Th2 反应和诱导 SSIAAD 的肿瘤坏死因子α和白细胞介素 17 反应来实现的。
大环内酯类在 AAD 中具有广泛的抗炎作用,可能与其抗菌作用无关。被抑制的特定反应取决于 AAD 期间占主导地位的反应。