Pathogenesis of nasal polyposis.

Pathogenesis of nasal polyposis.
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DOI:
10.1111/cea.12472
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发表时间:
2015-02
期刊:
Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
影响因子:
--
通讯作者:
Schleimer RP
Schleimer RP
中科院分区:
其他
文献类型:
--
作者:
Hulse KE;Stevens WW;Tan BK;Schleimer RP

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慢性鼻窦炎伴鼻息肉(CRSwNP)是一种复杂的炎症性疾病,影响世界范围内的大部分人口,并与高成本的管理和显着的发病率。然而,目前缺乏基于人群的流行病学研究,使用CRSwNP的当前定义,并且驱动这种疾病发病机制的机制仍不清楚。在这篇综述中,我们总结了目前的证据过多的因素,可能有助于CRSwNP的发病机制。气道上皮屏障的先天功能缺陷,包括抗微生物产品表达减少和屏障完整性丧失,以及真菌和细菌的定植可能在CRSwNP慢性炎症的发展中起关键作用。这种慢性炎症的特征在于许多关键炎性细胞因子和趋化因子的表达升高,包括IL-5、胸腺基质淋巴细胞生成素和CCL 11,其有助于启动和维持这种慢性炎症反应。总之,这些因素可能联合收割机驱动各种免疫细胞的流入,包括嗜酸性粒细胞、肥大细胞、第2组先天性淋巴样细胞和淋巴细胞,其参与鼻息肉内的慢性炎症反应。然而,重要的是,未来的研究需要证明这些潜在的疾病驱动因素在CRSwNP中的必要性和充分性。除了开发新的工具和模型来帮助机制研究之外,CRSwNP研究领域还需要为哮喘社区提供良好服务的强大流行病学数据。鉴于其高患病率、高成本和高发病率,非常需要对CRS进行持续研究,以促进开发新的治疗策略,改善对患有这种疾病的患者的治疗。
Chronic rhinosinusitis with nasal polyps (CRSwNP) is a complex inflammatory condition that affects a large proportion of the population world-wide and is associated with high cost of management and significant morbidity. Yet, there is a lack of population-based epidemiologic studies using current definitions of CRSwNP, and the mechanisms that drive pathogenesis in this disease remain unclear. In this review, we summarize the current evidence for the plethora of factors that likely contribute to CRSwNP pathogenesis. Defects in the innate function of the airway epithelial barrier, including diminished expression of antimicrobial products and loss of barrier integrity, combined with colonization by fungi and bacteria likely play a critical role in the development of chronic inflammation in CRSwNP. This chronic inflammation is characterized by elevated expression of many key inflammatory cytokines and chemokines, including IL-5, thymic stromal lymphopoietin and CCL11, that help to initiate and perpetuate this chronic inflammatory response. Together, these factors likely combine to drive the influx of a variety of immune cells, including eosinophils, mast cells, group 2 innate lymphoid cells and lymphocytes, which participate in the chronic inflammatory response within the nasal polyps. Importantly, however, future studies are needed to demonstrate the necessity and sufficiency of these potential drivers of disease in CRSwNP. In addition to the development of new tools and models to aid mechanistic studies, the field of CRSwNP research also needs the type of robust epidemiologic data that has served the asthma community so well. Given the high prevalence, costs and morbidity, there is a great need for continued research into CRS that could facilitate the development of novel therapeutic strategies to improve treatment for patients who suffer from this disease.
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