Fine particulate matter contributes to COPD-like pathophysiology: experimental evidence from rats exposed to diesel exhaust particles.
Fine particulate matter contributes to COPD-like pathophysiology: experimental evidence from rats exposed to diesel exhaust particles.
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细颗粒物有助于COPD样病理生理学：暴露于柴油机排气颗粒的大鼠的实验证据
DOI：
10.1186/s12931-023-02623-y
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发表时间：
2024-01-04
影响因子：
5.8
通讯作者：
中科院分区：
文献类型：
--
作者：
Ambient fine particulate matter (PM2.5) is considered a plausible contributor to the onset of chronic obstructive pulmonary disease (COPD). Mechanistic studies are needed to augment the causality of epidemiologic findings. In this study, we aimed to test the hypothesis that repeated exposure to diesel exhaust particles (DEP), a model PM2.5, causes COPD-like pathophysiologic alterations, consequently leading to the development of specific disease phenotypes. Sprague Dawley rats, representing healthy lungs, were randomly assigned to inhale filtered clean air or DEP at a steady-state concentration of 1.03 mg/m3 (mass concentration), 4 h per day, consecutively for 2, 4, and 8 weeks, respectively. Pulmonary inflammation, morphologies and function were examined. Black carbon (a component of DEP) loading in bronchoalveolar lavage macrophages demonstrated a dose-dependent increase in rats following DEP exposures of different durations, indicating that DEP deposited and accumulated in the peripheral lung. Total wall areas (WAt) of small airways, but not of large airways, were significantly increased following DEP exposures, compared to those following filtered air exposures. Consistently, the expression of α-smooth muscle actin (α-SMA) in peripheral lung was elevated following DEP exposures. Fibrosis areas surrounding the small airways and content of hydroxyproline in lung tissue increased significantly following 4-week and 8-week DEP exposure as compared to the filtered air controls. In addition, goblet cell hyperplasia and mucus hypersecretions were evident in small airways following 4-week and 8-week DEP exposures. Lung resistance and total lung capacity were significantly increased following DEP exposures. Serum levels of two oxidative stress biomarkers (MDA and 8-OHdG) were significantly increased. A dramatical recruitment of eosinophils (14.0-fold increase over the control) and macrophages (3.2-fold increase) to the submucosa area of small airways was observed following DEP exposures. DEP exposures over the courses of 2 to 8 weeks induced COPD-like pathophysiology in rats, with characteristic small airway remodeling, mucus hypersecretion, and eosinophilic inflammation. The results provide insights on the pathophysiologic mechanisms by which PM2.5 exposures cause COPD especially the eosinophilic phenotype. The online version contains supplementary material available at 10.1186/s12931-023-02623-y.
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影响因子：
5.6
作者：
Han H;Peng G;Meister M;Yao H;Yang JJ;Zou MH;Liu ZR;Ji X
通讯作者：
Ji X
影响因子：
3.7
作者：
Ghorani V;Boskabady MH;Khazdair MR;Kianmeher M
通讯作者：
Kianmeher M
影响因子：
10
作者：
Decaesteker T;Vanhoffelen E;Trekels K;Jonckheere AC;Cremer J;Vanstapel A;Dilissen E;Bullens D;Dupont LJ;Vanoirbeek JA
通讯作者：
Vanoirbeek JA
影响因子：
5.8
作者：
Karvonen HM;Lehtonen ST;Harju T;Sormunen RT;Lappi-Blanco E;Mäkinen JM;Laitakari K;Johnson S;Kaarteenaho RL
通讯作者：
Kaarteenaho RL
影响因子：
158.5
作者：
HOGG, JC;MACKLEM, PT;THURLBECK, WM
通讯作者：
THURLBECK, WM