A preclinical model to tackle chronic rhinosinusitis.

A preclinical model to tackle chronic rhinosinusitis.
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解决慢性鼻窦炎的临床前模型。

DOI:
10.1002/alr.22768
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发表时间:
2021
影响因子:
6.4
通讯作者:
Douglas,RichardG
Douglas,RichardG
中科院分区:
医学1区
文献类型:
--
作者:
Cho,Do-Yeon;Douglas,RichardG

文献摘要

相似文献

我们很高兴地阅读了Schilling及其同事最近的文章,我们赞扬作者在量化该临床前模型的放射学和组织学结果方面所做的努力。1正如作者在引言中指出的,慢性鼻窦炎(CRS)是一种多因素疾病过程,其特征是粘膜纤毛清除(MCC)受损,随后微生物清除受损。随后,由于骨道复合体阻塞引起的缺氧被广泛认为是导致慢性炎症的主要致病机制之一,并且这得到了以下证据的有力支持:缺氧存在于闭合口的患病窦的表面上皮。2我们已经研究这种基于阻塞的兔鼻窦炎模型超过五年,并希望评论文章中的几个发现。虽然没有一个单一的动物模型再现了人类疾病的所有特征,但一个良好控制的临床前模型可以提供一个回答人类疾病机制的机会。家兔和人鼻窦粘膜的免疫学特征相似,并建立了家兔急性鼻窦炎的动物模型。因此,我们使用兔作为慢性炎症的动物模型,通过阻塞窦流出道。3我们发现在第2周窦上皮细胞被急性炎症细胞(中性粒细胞)浸润。当再随访10至12周时,动物在第14周出现慢性炎症。这种基于阻塞的兔子模型可以提供一个前所未有的途径来研究微生物-宿主相互作用,其实验控制水平在人类中无法实现。
We were delighted to read the recent article by Schilling and colleagues and we commend the authors for their efforts in quantifying the radiography and histologic findings in this preclinical model. 1 As the authors pointed out in the introduction, chronic rhinosinusitis (CRS) is known to be a multifactorial disease process characterized by impaired mucociliary clearance (MCC) with subsequent compromised microbial elimination. Subsequently, hypoxia due to obstruction of the osteomeatal complex is widely considered one of the major pathogenic mechanisms leading to chronic inflammation, and this is strongly supported by evidence that hypoxia is present at the surface epithelium in diseased sinuses of closed ostia. 2 We have been studying this obstruction-based rabbit model of rhinosinusitis for more than half a decade and would like to comment on several findings in the article.Although no single animal model reproduces all the characteristics of human disease, a well-controlled preclinical model could provide an opportunity to answer the mechanisms in human diseases. Similarities exist between the immunologic features of rabbit and human sinus mucosa and an in vivo rabbit model of acute sinusitis has been established. Thus, we used rabbits as an animal model of chronic inflammation by blocking the sinus outflow tract. 3 We found that the sinus epithelium became infiltrated with acute inflammatory cells (neutrophils) during week 2. When followed for a further 10 to 12 weeks, the animals developed a chronic inflammatory condition by week 14. This obstruction-based rabbit model can provide an unprecedented gateway to study microbial-host interactions with a level of experimental control that is not achievable in humans.