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ADAM33 表达与慢性阻塞性肺疾病气道炎症的强相关性及其作为 COPD 生物标志物和治疗靶点的候选者。

The strong correlation between ADAM33 expression and airway inflammation in chronic obstructive pulmonary disease and candidate for biomarker and treatment of COPD.

机构信息

Department of Pulmonology and Respiratory Medicine, Faculty of Medicine and Health, Universitas Muhammadiyah, Jakarta, Indonesia.

Molecular Biology and Immunology Laboratory, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia.

出版信息

Sci Rep. 2021 Nov 30;11(1):23162. doi: 10.1038/s41598-021-02615-2.

DOI:10.1038/s41598-021-02615-2
PMID:34848800
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8632976/
Abstract

Airway inflammation in patients with chronic obstructive pulmonary disease (COPD) is an amplified response of the normal immune system that occurs as a result of chronic irritation by toxic substances, such as cigarette smoke. This leads to the characteristic pathological changes in the inflammatory cells of COPD patients. ADAM33 has been reported to be involved in the pathogenesis of COPD in East Asia by affecting airway inflammation and other immune responses. The aim of this study was to determine the potential role of ADAM33 (mRNA and soluble levels) as a biomarker of inflammation in COPD patients. This is a case control study using consecutive sampling. The COPD case and control (non-COPD) groups comprised 37 and 29 patients, respectively. We used univariate analysis to assess differences in the parameters between the groups and bivariate analysis to non-parametrically compare these parameters between the two groups. We observed significantly higher mRNA levels of ADAM33 in the COPD patients (10.39 ± 1.76) as compared to that in the non-COPD individuals (6.93 ± 0.39; P < 0.001). The levels of soluble ADAM33 were also significantly higher in the COPD patients (2.188 ± 1.142 ng/ml) compared to the non-COPD individuals (0.487 ± 0.105 ng/ml; P < 0.001). The mRNA and soluble ADAM33 levels were significantly higher in COPD patients compared to those in the parameter-matched non-COPD individuals. Thus, ADAM33 is a potential biomarker and treatment for inflammation in COPD patients.

摘要

慢性阻塞性肺疾病(COPD)患者的气道炎症是正常免疫系统的放大反应,是由有毒物质(如香烟烟雾)的慢性刺激引起的。这导致了 COPD 患者炎症细胞的特征性病理变化。ADAM33 已被报道通过影响气道炎症和其他免疫反应参与东亚 COPD 的发病机制。本研究旨在确定 ADAM33(mRNA 和可溶性水平)作为 COPD 患者炎症生物标志物的潜在作用。这是一项使用连续采样的病例对照研究。COPD 病例组和对照组(非 COPD 组)分别包括 37 例和 29 例患者。我们使用单变量分析评估了两组间参数的差异,并使用双变量分析对两组间这些参数进行了非参数比较。我们观察到 COPD 患者的 ADAM33 mRNA 水平明显高于非 COPD 个体(10.39±1.76 比 6.93±0.39;P<0.001)。可溶性 ADAM33 水平在 COPD 患者中也明显较高(2.188±1.142 ng/ml 比 0.487±0.105 ng/ml;P<0.001)。与参数匹配的非 COPD 个体相比,COPD 患者的 ADAM33 mRNA 和可溶性水平明显更高。因此,ADAM33 是 COPD 患者炎症的潜在生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa64/8632976/b0dd66cbb6af/41598_2021_2615_Fig8_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa64/8632976/b0dd66cbb6af/41598_2021_2615_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa64/8632976/41fe1afca5a2/41598_2021_2615_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa64/8632976/a0db9cde5714/41598_2021_2615_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa64/8632976/1a52e69741a8/41598_2021_2615_Fig6_HTML.jpg
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