{"title":"慢性柴油机废气暴露诱发肺血管重塑，这是交通相关肺动脉高压的潜在轨迹。","authors":"Chaohui Mu, Qinghai Li, Yong Niu, Ting Hu, Yanting Li, Tao Wang, Xinjuan Yu, Yiqiao Lv, Huiling Tang, Jing Jiang, Haibin Xu, Yuxin Zheng, Wei Han","doi":"10.1186/s12931-024-02976-y","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>As one of the most common traffic-related pollutants, diesel exhaust (DE) confers high risk for cardiovascular and respiratory diseases. However, its impact on pulmonary vessels is still unclear.</p><p><strong>Methods: </strong>To explore the effects of DE exposure on pulmonary vascular remodeling, our study analyzed the number and volume of small pulmonary vessels in the diesel engine testers (the DET group) from Luoyang Diesel Engine Factory and the controls (the non-DET group) from the local water company, using spirometry and carbon content in airway macrophage (CCAM) in sputum. And then we constructed a rat model of chronic DE exposure, in which 12 rats were divided into the DE group (6 rats with 16-week DE exposure) and the control group (6 rats with 16-week clean air exposure). During right heart catheterization, right ventricular systolic pressure (RVSP) was assessed by manometry. Macrophage migration inhibitory factor (MIF) in lung tissues and bronchoalveolar lavage fluid (BALF) were measured by qRT-PCR and ELISA, respectively. Histopathological analysis for cardiovascular remodeling was also performed.</p><p><strong>Results: </strong>In DET cohort, the number and volume of small pulmonary vessels in CT were positively correlated with CCAM in sputum (P<0.05). Rat model revealed that chronic DE-exposed rats had elevated RVSP, along with increased wall thickness of pulmonary small vessels and right the ventricle. What's more, the MIF levels in BALF and lung tissues were higher in DE-exposed rats than the controls.</p><p><strong>Conclusion: </strong>Apart from airway remodeling, DE also induces pulmonary vascular remodeling, which will lead to cardiopulmonary dysfunction.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"25 1","pages":"348"},"PeriodicalIF":5.8000,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439202/pdf/","citationCount":"0","resultStr":"{\"title\":\"Chronic diesel exhaust exposure induced pulmonary vascular remodeling a potential trajectory for traffic related pulmonary hypertension.\",\"authors\":\"Chaohui Mu, Qinghai Li, Yong Niu, Ting Hu, Yanting Li, Tao Wang, Xinjuan Yu, Yiqiao Lv, Huiling Tang, Jing Jiang, Haibin Xu, Yuxin Zheng, Wei Han\",\"doi\":\"10.1186/s12931-024-02976-y\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>As one of the most common traffic-related pollutants, diesel exhaust (DE) confers high risk for cardiovascular and respiratory diseases. 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引用次数: 0
摘要
背景：作为最常见的交通相关污染物之一，柴油废气（DE）具有引发心血管和呼吸系统疾病的高风险。然而，其对肺血管的影响仍不清楚：为了探讨柴油机废气暴露对肺血管重塑的影响，我们的研究利用肺活量测定法和痰液中的气道巨噬细胞含碳量（CCAM）分析了洛阳柴油机厂的柴油机测试者（DET组）和当地自来水公司的对照组（非DET组）的肺小血管数量和体积。然后，我们建立了慢性 DE 暴露大鼠模型，将 12 只大鼠分为 DE 组（6 只接触 DE 16 周）和对照组（6 只接触清洁空气 16 周）。在右心导管检查过程中，通过测压法评估了右心室收缩压（RVSP）。肺组织和支气管肺泡灌洗液（BALF）中的巨噬细胞迁移抑制因子（MIF）分别通过 qRT-PCR 和 ELISA 方法进行测定。此外，还对心血管重塑进行了组织病理学分析：结果：在 DET 队列中，CT 中肺部小血管的数量和体积与痰中的 CCAM 呈正相关：除气道重塑外，DE 还会诱发肺血管重塑，从而导致心肺功能障碍。
Chronic diesel exhaust exposure induced pulmonary vascular remodeling a potential trajectory for traffic related pulmonary hypertension.
Background: As one of the most common traffic-related pollutants, diesel exhaust (DE) confers high risk for cardiovascular and respiratory diseases. However, its impact on pulmonary vessels is still unclear.
Methods: To explore the effects of DE exposure on pulmonary vascular remodeling, our study analyzed the number and volume of small pulmonary vessels in the diesel engine testers (the DET group) from Luoyang Diesel Engine Factory and the controls (the non-DET group) from the local water company, using spirometry and carbon content in airway macrophage (CCAM) in sputum. And then we constructed a rat model of chronic DE exposure, in which 12 rats were divided into the DE group (6 rats with 16-week DE exposure) and the control group (6 rats with 16-week clean air exposure). During right heart catheterization, right ventricular systolic pressure (RVSP) was assessed by manometry. Macrophage migration inhibitory factor (MIF) in lung tissues and bronchoalveolar lavage fluid (BALF) were measured by qRT-PCR and ELISA, respectively. Histopathological analysis for cardiovascular remodeling was also performed.
Results: In DET cohort, the number and volume of small pulmonary vessels in CT were positively correlated with CCAM in sputum (P<0.05). Rat model revealed that chronic DE-exposed rats had elevated RVSP, along with increased wall thickness of pulmonary small vessels and right the ventricle. What's more, the MIF levels in BALF and lung tissues were higher in DE-exposed rats than the controls.
Conclusion: Apart from airway remodeling, DE also induces pulmonary vascular remodeling, which will lead to cardiopulmonary dysfunction.
期刊介绍：
Respiratory Research publishes high-quality clinical and basic research, review and commentary articles on all aspects of respiratory medicine and related diseases.
As the leading fully open access journal in the field, Respiratory Research provides an essential resource for pulmonologists, allergists, immunologists and other physicians, researchers, healthcare workers and medical students with worldwide dissemination of articles resulting in high visibility and generating international discussion.
Topics of specific interest include asthma, chronic obstructive pulmonary disease, cystic fibrosis, genetics, infectious diseases, interstitial lung diseases, lung development, lung tumors, occupational and environmental factors, pulmonary circulation, pulmonary pharmacology and therapeutics, respiratory immunology, respiratory physiology, and sleep-related respiratory problems.
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