Chronic exposure of diesel exhaust particles induces alveolar enlargement in mice
Respiratory tract
Alveolar macrophage
DOI:
10.1186/s12931-015-0172-z
Publication Date:
2015-02-06T04:04:03Z
AUTHORS (13)
ABSTRACT
Diesel exhaust particles (DEPs) are deposited into the respiratory tract and thought to be a risk factor for development of diseases system. In healthy individuals, timing mechanisms injuries caused by chronic exposure air pollution remain clarified.We evaluated effects DEP at doses below those found in typical bus corridor Sao Paulo (150 μg/m3). Male BALB/c mice were divided receiving nasal instillation: saline (saline; n = 30) 30 μg/10 μL (DEP; 30). Nasal instillations performed five days week, over period 90 days. Bronchoalveolar lavage (BAL) was performed, concentrations interleukin (IL)-4, IL-10, IL-13 interferon-gamma (INF-γ) determined ELISA-immunoassay. Assessment mechanics performed. The gene expression Muc5ac lung RT-PCR. presence IL-13, MAC2+ macrophages, CD3+, CD4+, CD8+ T cells CD20+ B tissues analysed immunohistochemistry. Bronchial thickness collagen/elastic fibers density morphometry. We measured mean linear intercept (Lm), measure alveolar distension, airspace diameter (D0) statistical distribution (D2).DEP decreased IFN-γ levels BAL (p 0.03), but did not significantly alter IL-4, IL-10 levels. macrophage, CD4+ cell numbers altered; however, CD3+ ≤ 0.001) increased parenchyma. Although 0.008) bronchiolar epithelium, altered DEP-exposed animals. mechanics, elastic collagen modified, (Lm) animals 0.001), index D2 statistically different 0.038) from control animals.Our data suggest that instillation low results enlargement pulmonary parenchyma mice.
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