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吸烟的慢性鼻-鼻窦炎伴哮喘患者鼻基质金属蛋白酶-1 和 -9 的表达增加。

Increased nasal matrix metalloproteinase-1 and -9 expression in smokers with chronic rhinosinusitis and asthma.

机构信息

Division of Rhinology, Department of Otolaryngology, Chang Gung Memorial Hospital and Chang Gung University, Taoyuan, Taiwan.

Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan.

出版信息

Sci Rep. 2019 Oct 25;9(1):15357. doi: 10.1038/s41598-019-51813-6.

DOI:10.1038/s41598-019-51813-6
PMID:31653934
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6814857/
Abstract

A potential mechanism underlying cigarette smoke-induced airway disease is insufficient tissue repair via altered production of matrix metalloproteinases (MMPs). Osteitis is a signature feature of recalcitrant chronic rhinosinusitis (CRS) and often results in revision surgery. The present study aimed to investigate MMP expression in the nasal tissues of asthmatic patients with CRS and any association with cigarette smoking and osteitis. Thirteen smokers with CRS and asthma, 16 non-smokers with CRS and asthma, and seven non-smoker asthmatic patients without CRS were prospectively recruited. The expression of MMPs and associated immunological factors in surgically-obtained nasal tissues was evaluated via real-time PCR and western blotting. Maximal bone thickness of the anterior ethmoid (AE) partition was measured in axial sinus computed tomography (CT) sections. MMP-1 and MMP-9 expression was increased in the nasal tissues of smokers with asthma and CRS via real-time PCR and western blot. Maximal AE partition bone thickness was greater in smokers with CRS and asthma than in non-smokers with CRS and asthma. MMP-1 and MMP-9 levels were correlated with maximal AE bone thickness. Cigarette smoking was associated with the up-regulation of MMP-1 and MMP-9 in the nasal tissues of patients with airway inflammatory diseases, and with AE osteitis, and with therapeutic resistence.

摘要

烟雾引起气道疾病的一个潜在机制是基质金属蛋白酶(MMPs)产生改变导致组织修复不足。骨炎是难治性慢性鼻-鼻窦炎(CRS)的一个标志性特征,常导致手术修正。本研究旨在调查 MMP 在哮喘合并 CRS 患者鼻组织中的表达情况,以及其与吸烟和骨炎的任何关联。前瞻性招募了 13 名吸烟合并 CRS 和哮喘的患者、16 名非吸烟合并 CRS 和哮喘的患者以及 7 名无 CRS 的非吸烟哮喘患者。通过实时 PCR 和 Western blot 评估手术获得的鼻组织中 MMPs 及相关免疫因子的表达。在轴向鼻窦 CT 切片中测量前筛板(AE)分区的最大骨厚度。通过实时 PCR 和 Western blot 发现,吸烟合并哮喘和 CRS 的患者鼻组织中 MMP-1 和 MMP-9 的表达增加。吸烟合并 CRS 和哮喘的患者的 AE 分区最大骨厚度大于非吸烟合并 CRS 和哮喘的患者。MMP-1 和 MMP-9 水平与 AE 最大骨厚度相关。吸烟与气道炎症疾病患者鼻组织中 MMP-1 和 MMP-9 的上调以及 AE 骨炎和治疗抵抗有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93ac/6814857/d2bfbcdec0f6/41598_2019_51813_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93ac/6814857/d2e813709947/41598_2019_51813_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93ac/6814857/f79fcb9b76d4/41598_2019_51813_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93ac/6814857/31feb9f1c9e3/41598_2019_51813_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93ac/6814857/8cc1c91848b3/41598_2019_51813_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93ac/6814857/d2bfbcdec0f6/41598_2019_51813_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93ac/6814857/d2e813709947/41598_2019_51813_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93ac/6814857/f79fcb9b76d4/41598_2019_51813_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93ac/6814857/31feb9f1c9e3/41598_2019_51813_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93ac/6814857/8cc1c91848b3/41598_2019_51813_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93ac/6814857/d2bfbcdec0f6/41598_2019_51813_Fig5_HTML.jpg

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