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几丁质酶在与烟草烟雾暴露相关的慢性气道炎症中的作用。

The Role of Chitinases in Chronic Airway Inflammation Associated with Tobacco Smoke Exposure.

机构信息

Department of Internal Medicine, Pulmonary Diseases and Allergy, Medical University of Warsaw, 02-097 Warsaw, Poland.

Postgraduate School of Molecular Medicine, Medical University of Warsaw, 02-097 Warsaw, Poland.

出版信息

Cells. 2022 Nov 25;11(23):3765. doi: 10.3390/cells11233765.

DOI:10.3390/cells11233765
PMID:36497025
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9736934/
Abstract

Chitinases and chitinase-like proteins are thought to play a role in innate inflammatory responses. Our study aimed to assess whether chitinase concentration and activity in induced sputum (IS) of patients exposed to tobacco smoke are related to the level of airway inflammation including the level and activity of chitinases and chitinase-like proteins. The study included 22 patients with chronic obstructive pulmonary disease (COPD), 12 non-COPD smokers, and nine nonsmoking subjects. Sputum CHIT1 and YKL-40 levels and chitinolytic activity were compared with sputum IL-6, IL-8, IL-18, and MMP-9 levels. A hierarchical cluster analysis was also performed. Sputum YKL-40 was higher in COPD patients than in the control groups. Sputum CHIT1 and YKL-40 levels correlated with IS inflammatory cell count as well as with MMP-9 and IL-8 levels. Two main clusters were revealed: Cluster 1 had lower chitinase levels and activity, lower IS macrophage and neutrophil count, and lower IS IL-8, IL-18, and MMP-9 than Cluster 2. Comparison of COPD patients from both clusters revealed significant differences in the IS inflammatory profile despite comparable clinical and functional data. Our findings seem to confirm the involvement of chitinases in smoking-associated chronic airway inflammation and show that airway chitinases may be a potential novel marker in COPD phenotyping.

摘要

几丁质酶和几丁质酶样蛋白被认为在先天炎症反应中发挥作用。我们的研究旨在评估暴露于烟草烟雾的患者诱导痰(IS)中的几丁质酶浓度和活性是否与气道炎症水平相关,包括几丁质酶和几丁质酶样蛋白的水平和活性。该研究纳入了 22 名慢性阻塞性肺疾病(COPD)患者、12 名非 COPD 吸烟者和 9 名非吸烟者。比较了 IS 中 CHIT1 和 YKL-40 水平和几丁质裂解活性与 IL-6、IL-8、IL-18 和 MMP-9 水平。还进行了层次聚类分析。COPD 患者的 IS 中 YKL-40 高于对照组。IS 中 CHIT1 和 YKL-40 水平与 IS 炎性细胞计数以及 MMP-9 和 IL-8 水平相关。揭示了两个主要聚类:聚类 1 具有较低的几丁质酶水平和活性,较低的 IS 巨噬细胞和中性粒细胞计数,以及较低的 IS IL-8、IL-18 和 MMP-9 水平,而聚类 2 则相反。尽管临床和功能数据相似,但对两个聚类中的 COPD 患者进行比较显示,IS 炎症特征存在显著差异。我们的研究结果似乎证实了几丁质酶参与吸烟相关的慢性气道炎症,并表明气道几丁质酶可能是 COPD 表型的潜在新型标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fff0/9736934/da6ee2e740ca/cells-11-03765-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fff0/9736934/9157ea8e2414/cells-11-03765-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fff0/9736934/78f38e80cf28/cells-11-03765-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fff0/9736934/da6ee2e740ca/cells-11-03765-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fff0/9736934/9157ea8e2414/cells-11-03765-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fff0/9736934/78f38e80cf28/cells-11-03765-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fff0/9736934/da6ee2e740ca/cells-11-03765-g003.jpg

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Inhibition of CHIT1 as a novel therapeutic approach in idiopathic pulmonary fibrosis.
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