Diesel exhaust particles stimulate human airway epithelial cells to produce cytokines relevant to airway inflammation in vitro☆,☆☆,★,★★
Section snippets
Preparation of SPM and DEPs
SPM was collected by using a high-volume air sampler (Andersen type, Model AH-600; Sibata Scientific Technology Ltd., Tokyo, Japan). The air sampler was set up at a polluted district in the Tokyo metropolitan area and operated for 6 consecutive days.7 The materials collected during February and March 1987 were pooled and stored at 4° C. The principles of the classification of particles in this instrument were reported previously.16 We used SPM with sizes ranging from 7.0 μm to 10 μm.
The engine
SPM and DEPs stimulated airway epithelial cells to release GM-CSF, IL-8, or both
As shown in Fig. 1, A, SPM at 250 μg/ml had a significant stimulatory effect on GM-CSF release from human upper airway epithelial cells in a time-dependent fashion.
Discussion
In this report we found that DEPs, one of the important air pollutants, stimulated cytokine production by human airway epithelial cells (Table I).
Pollutants Epithelial cells GM-CSF production IL-8 production SPM Nasal ↑ → Bronchial ↑ → BEAS-2B ↑ → DEPs Nasal ↑ ↑ Bronchial ↑ ↑ BEAS-2B ↑ ↑ Benzo(a)pyrene BEAS-2B ↑ ↑
Acknowledgements
We thank Dr. M. Sagai for his kind supply of DEPs and Ms. Chinami Sakamaki and Asako Hashimoto for their excellent technical support.
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2023, Environmental PollutionCitation Excerpt :Many studies have shown that DEPs can increase the expression of genes involved in immune or inflammatory responses, such as cytokines and chemokines, in lung cells (Schwarze et al., 2013). DEPs can significantly increase the production of cytokines such as interleukin (IL)-8 and granulocyte-macrophage colony-stimulating factor in human airway epithelial cells (Ohtoshi et al., 1998). In addition, expression levels of various cytokines such as tumor necrosis factor, IL-6, and monocyte chemoattractant protein-1 are increased in the lungs of mice exposed to DEPs (Saber et al., 2006).
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2019, Science of the Total EnvironmentCitation Excerpt :ROS formed on the surfaces of particles activate either antioxidant defense mechanisms (at low levels of oxidative stress), inflammatory responses (at intermediate levels of oxidative stress) or cytotoxic effects (at high levels of oxidative stress) (Steiner et al., 2016; Xiao et al., 2003). It is known that DEP increase oxidative stress and influence human bronchial epithelial cell-dendritic cell interactions via cytokines including thymic stromal lymphopoietin (TSLP) (Reibman et al., 2003; Ohtoshi et al., 1998; Boland et al., 1999; Reibman et al., 2002; Bleck et al., 2008; Liu et al., 2007). Bleck et al. (Bleck et al., 2010), using primary culture human bronchial epithelial cells, proposed that DEP-treated cells upregulate Jagged-1 and OX40L in myeloid dendritic cells via TSLP, resulting in functional dendritic cells that support Th2 polarization, although this theory has never been demonstrated in vivo.
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From athe Departments of Medicine and Physical Therapy and bthe Department of Otolaryngology, University of Tokyo, School of Medicine, Tokyo; and cthe Department of Internal Medicine, University of Teikyo, School of Medicine, Tokyo.
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Supported in part by The Manabe Medical Foundation.
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Reprint requests: Hajime Takizawa, MD, PhD, Department of Medicine and Physical Therapy, University of Tokyo, School of Medicine, 7-3-1 Hongo, Bunkyo-ku, 113 Japan.
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