Diesel exhaust enhances influenza virus infections in respiratory epithelial cells

被引:134
作者
Jaspers, I
Ciencewicki, JM
Zhang, WL
Brighton, LE
Carson, JL
Beck, MA
Madden, MC
机构
[1] Univ N Carolina, CEMALB, Chapel Hill, NC 27599 USA
[2] Univ N Carolina, Curriculum Toxicol, Chapel Hill, NC 27599 USA
[3] Univ N Carolina, Dept Pediat, Div Infect Dis & Host Def, Chapel Hill, NC 27599 USA
[4] US EPA, Human Studies Div, Chapel Hill, NC 27599 USA
关键词
influenza; diesel exhaust; in vitro; epithelial cells; oxidative stress;
D O I
10.1093/toxsci/kfi141
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Several factors, such as age and nutritional status, can affect the susceptibility to influenza infections. Moreover, exposure to air pollutants, such as diesel exhaust (DE), has been shown to affect respiratory virus infections in rodent models. Influenza virus primarily infects and replicates in respiratory epithelial cells, which are also a major targets for inhaled DE. Using in vitro models of human respiratory epithelial cells, we determined the effects of an aqueous-trapped solution of DE (DEas) on influenza infections. Differentiated human nasal and bronchial epithelial cells, as well as A549 cells, were exposed to DEas and infected with influenza A/Bangkok/1/79. DEas enhanced the susceptibility to influenza virus infection in all cell models and increased the number of influenza-infected cells within 24 h post-infection. This was not caused by suppressing antiviral mediator production, since interferon (IFN) beta levels, IFN-dependent signaling, and IFN-stimulated gene expression were also enhanced by exposure to DEas. Many of the adverse effects induced by DE exposure are mediated by oxidative stress. Exposure to DEas used in these studies generated oxidative stress in respiratory epithelial cells, and addition of the antioxidant glutathione-ethylester (GSH-ET) reversed the effects of DEas on influenza infections. Furthermore, DEas increased influenza virus attachment to respiratory epithelial cells within 2 h post-infection. Taken together, the results presented here suggest that in human respiratory epithelial cells oxidative stress generated by DEas increases the susceptibility to influenza infection and that exposure to DEas increases the ability of the virus to attach to and enter respiratory epithelial cells.
引用
收藏
页码:990 / 1002
页数:13
相关论文
共 64 条
[1]   Expression of cytokines on human bronchial epithelial cells induced by influenza virus A [J].
Adachi, M ;
Matsukura, S ;
Tokunaga, H ;
Kokubu, F .
INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY, 1997, 113 (1-3) :307-311
[2]   Selenium deficiency increases the pathology of an influenza virus infection [J].
Beck, MA ;
Nelson, HK ;
Shi, Q ;
Van Dael, P ;
Schiffrin, EJ ;
Blum, S ;
Barclay, D ;
Levander, OA .
FASEB JOURNAL, 2001, 15 (06) :1481-+
[3]   Micronutrients and host resistance to viral infection [J].
Beck, MA ;
Matthews, CC .
PROCEEDINGS OF THE NUTRITION SOCIETY, 2000, 59 (04) :581-585
[4]   Organic compounds from diesel exhaust particles elicit a proinflammatory response in human airway epithelial cells and induce cytochrome p450 1A1 expression [J].
Bonvallot, V ;
Baeza-Squiban, A ;
Baulig, A ;
Brulant, S ;
Boland, S ;
Muzeau, F ;
Barouki, R ;
Marano, F .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2001, 25 (04) :515-521
[5]   Inhibition of influenza infection by glutathione [J].
Cai, JY ;
Chen, Y ;
Seth, S ;
Furukawa, S ;
Compans, RW ;
Jones, DP .
FREE RADICAL BIOLOGY AND MEDICINE, 2003, 34 (07) :928-936
[6]   Effect of exposure to diesel exhaust particles on the susceptibility of the lung to infection [J].
Castranova, V ;
Ma, JYC ;
Yang, HM ;
Antonini, JM ;
Butterworth, L ;
Barger, MW ;
Roberts, J ;
Ma, JKH .
ENVIRONMENTAL HEALTH PERSPECTIVES, 2001, 109 :609-612
[7]   Human SLPI inactivation after cigarette smoke exposure in a new in vivo model of pulmonary oxidative stress [J].
Cavarra, E ;
Lucattelli, M ;
Gambelli, F ;
Bartalesi, B ;
Fineschi, S ;
Szarka, A ;
Giannerini, F ;
Martorana, PA ;
Lungarella, G .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2001, 281 (02) :L412-L417
[8]   REGULATION OF CILIATED CELL-DIFFERENTIATION IN CULTURES OF RAT TRACHEAL EPITHELIAL-CELLS [J].
CLARK, AB ;
RANDELL, SH ;
NETTESHEIM, P ;
GRAY, TE ;
BAGNELL, B ;
OSTROWSKI, LE .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1995, 12 (03) :329-338
[9]  
D'Amato G, 2002, Monaldi Arch Chest Dis, V57, P136
[10]  
DiazSanchez D, 1997, ALLERGY, V52, P52