Biological Responses to Diesel Exhaust Particles (DEPs) Depend on the Physicochemical Properties of the DEPs

被引:17
作者
Park, Eun-Jung [1 ]
Roh, Jinkyu [2 ]
Kang, Min-Sung [3 ]
Kim, Soo Nam [3 ]
Kim, Younghun [2 ]
Choi, Sangdun [1 ]
机构
[1] Ajou Univ, Dept Mol Sci & Technol, Suwon 441749, South Korea
[2] Kwangwoon Univ, Dept Chem Engn, Seoul, South Korea
[3] Korea Inst Toxicol, Inhalat Toxicol Ctr, Jeongeup, South Korea
来源
PLOS ONE | 2011年 / 6卷 / 10期
基金
新加坡国家研究基金会;
关键词
GROWTH-FACTOR-BETA; P53; HYDROCARBONS; INFLAMMATION; PARTICULATE; EXPRESSION; INDUCTION; DAMAGE; COX-2; DNA;
D O I
10.1371/journal.pone.0026749
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Diesel exhaust particles (DEPs) are the main components of ambient particulate materials, including polyaromatic hydrocarbons (PAHs), n-PAHs, heavy metals, and gaseous materials. Many epidemiological, clinical, and toxicological studies have shown that ambient particles, including DEPs, are associated with respiratory disorders, such as asthma, allergic rhinitis, and lung cancer. However, the relationship between the biological response to DEPs and their chemical composition remains unclear. In this study, we investigated the physicochemical properties of DEPs before toxicological studies, and then administered a single intratracheal instillation of DEPs to mice. The mice were then killed 1, 7, 14 and 28 days after DEP exposure to observe the biological responses induced by DEPs over time. Our findings suggest that DEPs engulfed into cells induced a Th2-type inflammatory response followed by DNA damage, whereas DEPs not engulfed into cells induced a Th1-type inflammatory response. Further, the physicochemical properties, including surface charge, particle size, and chemical composition, of DEPs play a crucial role in determining the biological responses to DEPs. Consequently, we suggest that the biological response to DEPs depend on cell-particle interaction and the physicochemical properties of the particles.
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页数:10
相关论文
共 33 条
  • [1] Mutagenicity of diesel exhaust particles mediated by cell-particle interaction in mammalian cells
    Bao, Lingzhi
    Chen, Shaopeng
    Wu, Lijun
    Hei, Tom K.
    Wu, Yuejin
    Yu, Zengliang
    Xu, An
    [J]. TOXICOLOGY, 2007, 229 (1-2) : 91 - 100
  • [2] Mechanisms of disease:: Role of transforming growth factor β in human disease.
    Blobe, GC
    Schiemann, WP
    Lodish, HF
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (18) : 1350 - 1358
  • [3] Differential Impact of Diesel Particle Composition on Pro-allergic Dendritic Cell Function
    Braun, Andrea
    Bewersdorff, Mayte
    Lintelmann, Jutta
    Matuschek, Georg
    Jakob, Thilo
    Goettlicher, Martin
    Schober, Wolfgang
    Buters, Jeroen T. M.
    Behrendt, Heidrun
    Mempel, Martin
    [J]. TOXICOLOGICAL SCIENCES, 2010, 113 (01) : 85 - 94
  • [4] COX-2 expression induced by diesel particles involves chromatin modification and degradation of HDAC1
    Cao, Dongsun
    Bromberg, Philip A.
    Samet, James M.
    [J]. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2007, 37 (02) : 232 - 239
  • [5] Chiarugi V, 1998, INT J MOL MED, V2, P715
  • [6] DiazSanchez D, 1997, ALLERGY, V52, P52
  • [7] Wilms tumor gene (WT1) and p53 expression in endometrial carcinomas: a study of 130 cases using a tissue microarray
    Dupont, J
    Wang, X
    Marshall, DS
    Leitao, M
    Hedvat, CV
    Hummer, A
    Thaler, H
    O'Reilly, RJ
    Soslow, RA
    [J]. GYNECOLOGIC ONCOLOGY, 2004, 94 (02) : 449 - 455
  • [8] Convergence of p53 and TGF-beta signaling networks
    Dupont, S
    Zacchigna, L
    Adorno, M
    Soligo, S
    Volpin, D
    Piccolo, S
    Cordenonsi, M
    [J]. CANCER LETTERS, 2004, 213 (02) : 129 - 138
  • [9] Effects of Diesel Exhaust Particles on Antigen-Presenting Cells and Antigen-Specific Th Immunity in Mice
    Inoue, Ken-ichiro
    Koike, Eiko
    Takano, Hirohisa
    Yanagisawa, Rie
    Ichinose, Takamichi
    Yoshikawa, Toshikazu
    [J]. EXPERIMENTAL BIOLOGY AND MEDICINE, 2009, 234 (02) : 200 - 209
  • [10] Janeway C, 2005, IMMUNOBIOLOGY IMMUNE, Vxxiii