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过敏在鼻息肉病中的作用:综述

Role of allergy in nasal polyposis: a review.

作者信息

Bernstein J M, Gorfien J, Noble B

机构信息

Department of Otolaryngology, State University of New York at Buffalo, USA.

出版信息

Otolaryngol Head Neck Surg. 1995 Dec;113(6):724-32. doi: 10.1016/s0194-5998(95)70012-9.

DOI:10.1016/s0194-5998(95)70012-9
PMID:7501384
Abstract

We propose a multivariate theory for the pathogenesis of nasal polyps. Turbulent flow of air in the lateral wall of the nose or viral-bacterial-host interactions produce an inflammatory change in the mucosa of the lateral wall of the nose. Ulceration and prolapse of the submucosa with reepithelialization and new gland formation may then follow. The structural cells of the nasal polyp, including epithelial cells and fibroblasts, have the ability to produce messenger RNA for granulocyte-monocyte colony-stimulating factor and other cytokines. Stimulation of such an effector capability by structural cell-derived cytokines would undoubtedly represent a major amplification pathway of the inflammatory response in nasal polyps. Allergy may be one mechanism for the development of this cascade of events. This microenvironmental structural inflammatory response in the nasal polyp, in turn, can affect the bioelectric integrity of the Na+ and Cl- channels at the luminal surface of the respiratory epithelial cell. The change in the Na+ absorption, which has been demonstrated in our studies, may result in an increased movement of water into the cell and into the interstitial fluid. The resultant edema can lead to growth and enlargement of the nasal polyp. Finally, the rapid recurrence of nasal polyps despite adequate surgery may reflect some intrinsic phenotypic characteristic of nasal epithelial cells in the lateral wall of the nose, which is likely to be under genetic control.

摘要

我们提出了一种鼻息肉发病机制的多变量理论。鼻腔外侧壁的气流紊乱或病毒 - 细菌与宿主的相互作用会导致鼻腔外侧壁黏膜发生炎症变化。随后可能会出现黏膜下层的溃疡和脱垂,并伴有再上皮化和新腺体形成。鼻息肉的结构细胞,包括上皮细胞和成纤维细胞,有能力产生粒细胞 - 单核细胞集落刺激因子和其他细胞因子的信使核糖核酸。结构细胞衍生的细胞因子对这种效应能力的刺激无疑将代表鼻息肉炎症反应的主要放大途径。过敏可能是这一系列事件发生的一种机制。鼻息肉中的这种微环境结构炎症反应反过来又会影响呼吸道上皮细胞腔表面钠和氯通道的生物电完整性。我们的研究已证实,钠吸收的变化可能导致更多水分进入细胞和间质液。由此产生的水肿可导致鼻息肉生长和增大。最后,尽管进行了充分的手术,鼻息肉仍迅速复发,这可能反映了鼻腔外侧壁鼻上皮细胞的一些内在表型特征,而这很可能受基因控制。

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