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標題: Motorcycle exhaust particles augment antigen-induced airway inflammation in BALB/c mice
作者: Lee, C.C.
Cheng, Y.W.
Liao, J.W.
Chiang, B.L.
Lai, Y.L.
Kang, J.J.
關鍵字: activated protein-kinase;diesel exhaust;in-vivo;t-cells;unrestrained;plethysmography;adjuvant activity;epithelial-cells;disease severity;ige production;asthma
Project: Journal of Toxicology and Environmental Health-Part a-Current Issues
期刊/報告no:: Journal of Toxicology and Environmental Health-Part a-Current Issues, Volume 71, Issue 6, Page(s) 405-412.
Evidence indicates that environment pollutants from fossil fuel combustion compromise the immune system by enhancing allergic reactions and damaging the respiratory tract. This study was performed to investigate the effects of motorcycle exhaust particles (MEP), a major air pollutant especially in the urban areas of Taiwan, on allergen-induced airway inflammatory reactions in lab animals. BALB/c mice were intratracheally instilled with ovalbumin (OVA), MEP, or phosphate-buffered saline, 3 times every 2 wk. Airway hyperresponsiveness was measured in unrestrained mice by barometric plethsmography. Bronchoalveolar lavage fluid (BALF) and serum from treated animals were collected for cytokine and antibody determination by enzyme-linked immunosorbent assay (ELISA). Lung tissue stained with hematoxylin/eosin was examined. Data showed that MEP augmented OVA-induced airway inflammation; characterized by infiltration of eosinophils and neutrophils in BALF and lung tissue inflammation. The combination of OVA and MEP markedly increased interleukin-4 (IL-4), interleukin-5 (IL-5), and tumor necrosis factor-alpha(TNF-alpha) protein levels in BALF. In addition, MEP also augmented OVA-induced rise in OVA-specific immunoglobulin (Ig) G1 and IgE and airway hyperresponsiveness. Pretreated lavage cells with mitogen-activated protein kinase (MAPK) inhibitors showed that TNF-alpha release was significantly inhibited. This study found that MEP augmented antigen-induced allergic airway inflammation and airway hyperresponsiveness through a Th2-dominant pathway.
ISSN: 1528-7394
DOI: 10.1080/15287390701801687
Appears in Collections:獸醫病理生物學所

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