Role of IL-18 in Second-Hand Smoke-Induced Emphysema

被引:41
作者
Kratzer, Adelheid [1 ]
Salys, Jonas [1 ]
Nold-Petry, Claudia [2 ]
Cool, Carlyne [1 ]
Zamora, Martin [1 ]
Bowler, Russ [3 ]
Koczulla, Andreas Rembert [4 ]
Janciauskiene, Sabina [5 ]
Edwards, Michael G. [1 ]
Dinarello, Charles A. [2 ]
Taraseviciene-Stewart, Laimute [1 ]
机构
[1] Univ Colorado Denver, Dept Med, Div Pulm Sci & Crit Care Med, Aurora, CO 80045 USA
[2] Univ Colorado Denver, Dept Med, Div Infect Dis, Aurora, CO 80045 USA
[3] Natl Jewish Hlth, Denver, CO USA
[4] Univ Clin Giessen & Marburg, Dept Med, Marburg, Germany
[5] Hannover Med Sch, Dept Resp Med, Hannover, Germany
基金
美国国家卫生研究院;
关键词
second-hand cigarette smoke; emphysema; inflammation; macrophages; vasculature; CIGARETTE-SMOKE; PULMONARY-HYPERTENSION; PASSIVE SMOKING; BINDING-PROTEIN; RESPIRATORY SYMPTOMS; POLICY STATEMENT; IFN-GAMMA; INFLAMMATION; PATHOGENESIS; INTERLEUKIN-18;
D O I
10.1165/rcmb.2012-0173OC
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chronic second-hand smoke (SHS) exposure comprises the main risk factor for nonsmokers to develop chronic obstructive pulmonary disease (COPD). However, the mechanisms behind the chronic inflammation and lung destruction remain incompletely understood. In this study, we show that chronic exposure of Sprague-Dawley rats to SHS results in a significant increase of proinflammatory cytokine IL-18 and chemokine (C-C motif) ligand 5 in the bronchoalveolar lavage fluid (BALF) and a significant decrease of vascular endothelial growth factor (VEGF) in the lung tissue. SHS exposure resulted in progressive alveolar airspace enlargement, cell death, pulmonary vessel loss, vessel muscularization, collagen deposition, and right ventricular hypertrophy. Alveolar macrophages displayed a foamy phenotype and a decreased expression of the natural inhibitor of IL-18, namely, IL-18 binding protein (IL-18BP). Moreover, IL-18 down-regulated the expression of VEGF receptor-1 and VEGFR receptor-2, and induced apoptosis in pulmonary microvascular endothelial cells in vitro. We also observed a trend toward increased concentrations of IL-18 in the BALF of patients with COPD. Our findings suggest that IL-18-mediated endothelial cell death may contribute to vascular destruction and disappearance in SHS-induced COPD. Moreover, IL-18 and IL-18BP are potential new targets for therapeutics.
引用
收藏
页码:725 / 732
页数:8
相关论文
共 50 条
[31]   Role of carbon monoxide in impaired endothelial function mediated by acute second-hand tobacco, incense, and candle smoke exposures [J].
Weber, Lynn P. ;
Al-Dissi, Ahmad ;
Marit, Jordan S. ;
German, Timothy N. ;
Terletski, Sharilyn D. .
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, 2011, 31 (03) :453-459
[32]   CircRNA_0026344 via miR-21 is involved in cigarette smoke-induced autophagy and apoptosis of alveolar epithelial cells in emphysema [J].
Zhao, Jing ;
Xia, Haibo ;
Wu, Yan ;
Lu, Lu ;
Cheng, Cheng ;
Sun, Jing ;
Xiang, Quanyong ;
Bian, Tao ;
Liu, Qizhan .
CELL BIOLOGY AND TOXICOLOGY, 2023, 39 (03) :929-944
[33]   Comparison of Serum Adiponectin in Smoke-induced Pulmonary Emphysema Rats Fed Different Diets [J].
Wang, Rui-Ying ;
Liu, Hu ;
Ma, Li-Juan ;
Xu, Jian-Ying .
CHINESE MEDICAL JOURNAL, 2016, 129 (02) :187-193
[34]   Role of tumour necrosis factor-α receptor p75 in cigarette smoke-induced pulmonary inflammation and emphysema [J].
D'hulst, A. I. ;
Bracke, K. R. ;
Maes, T. ;
De Bleecker, J. L. ;
Pauwels, R. A. ;
Joos, G. F. ;
Brusselle, G. G. .
EUROPEAN RESPIRATORY JOURNAL, 2006, 28 (01) :102-112
[35]   Multiple sclerosis, seizures, and antiepileptics: role of IL-18, IDO, and melatonin [J].
Anderson, G. ;
Rodriguez, M. .
EUROPEAN JOURNAL OF NEUROLOGY, 2011, 18 (05) :680-685
[36]   Pressure overload induces IL-18 and IL-18R expression, but markedly suppresses IL-18BP expression in a rabbit model. IL-18 potentiates TNF-α-induced cardiomyocyte death [J].
Yoshida, Tadashi ;
Friehs, Ingeborg ;
Mummidi, Srinivas ;
del Nido, Pedro J. ;
Addulnour-Nakhoul, Solange ;
Delafontaine, Patrice ;
Valente, Anthony J. ;
Chandrasekar, Bysani .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2014, 75 :141-151
[37]   Second-hand smoke - a license to kill due to expire [J].
Narkiewicz, Krzysztof .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2007, 22 (06) :1508-1511
[38]   Infiltration of IL-17-Producing T Cells and Treg Cells in a Mouse Model of Smoke-Induced Emphysema [J].
Min-Chao Duan ;
Jian-Quan Zhang ;
Yue Liang ;
Guang-Nan Liu ;
Jin Xiao ;
Hai-Juan Tang ;
Yi Liang .
Inflammation, 2016, 39 :1334-1344
[39]   The effect of long-term doxycycline treatment in a mouse model of cigarette smoke-induced emphysema and pulmonary hypertension [J].
Hadzic, Stefan ;
Wu, Cheng-Yu ;
Gredic, Marija ;
Kojonazarov, Baktybek ;
Pak, Oleg ;
Kraut, Simone ;
Sommer, Natascha ;
Kosanovic, Djuro ;
Grimminger, Friedrich ;
Schermuly, Ralph T. ;
Seeger, Werner ;
Bellusci, Saverio ;
Weissmann, Norbert .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2021, 320 (05) :L903-L915
[40]   The influence of 5-lipoxygenase on cigarette smoke-induced emphysema in mice [J].
Kennedy-Feitosa, Emanuel ;
Santos Pinto, Romulo Fonseca ;
Pereira Pires, Karla Maria ;
Teixeira Monteiro, Ana Paula ;
Machado, Mariana Nascimento ;
Santos, Juliana Carvalho ;
Ribeiro, Marcelo Lima ;
Zin, Walter Araujo ;
Canetti, Claudio Azevedo ;
Romana-Souza, Bruna ;
Porto, Luis Cristovao ;
Valenca, Samuel Santos .
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, 2014, 1840 (01) :199-208