Diesel Exhaust Particles
Diesel Exhaust Particles
Purpose of Review: It has been demonstrated that particulate air pollutants such as diesel exhaust particles (DEPs) are associated with allergic respiratory disorders, including asthma and allergic rhinitis. Recent in-vivo and in-vitro studies strongly suggest that DEPs induce both anti-inflammatory and proinflammatory products by activating their transcription. If pollutants are to be controlled in the environment in a cost-effective manner, it is important that the molecular target(s) of DEP-induced responses be elucidated. Bronchial epithelial cells are the key regulators of airway inflammation, and therefore it is crucial to clarify the cellular and molecular mechanisms that are active in these cells. It is also important to compare responses to DEP exposure between healthy and susceptible populations.
Recent Findings: Studies have shown that DEPs activate several signalling pathways such as mitogen-activated protein kinases and transcription factors, in particular nuclear factor-μ and activator protein-1, in human bronchial epithelial cells; these effects are thought to occur via production of reactive oxygen species. Antioxidants effectively reduce the allergic inflammatory effects of DEPs both in vitro and in mice.
Summary: Host responses to DEPs are regulated by a balance between antioxidants and proinflammatory responses. DEP-induced oxidants play a key role in proinflammatory reactions. Recent human studies suggest that chemoprevention against DEP-induced adverse effects in susceptible individuals is possible.
The prevalence of asthma has been increasing in most industrialized countries of the world. Persistent exposure to particulate air pollution from motor vehicles has been implicated as one of the factors that are responsible for the increased prevalence of allergic diseases. Because diesel exhaust particles (DEPs) are the major component of ambient fine particulate matter [i.e. particulate matter of diameter <2.5 µm (PM2.5)], especially in urban areas, many in-vivo and in-vitro studies have been performed to clarify the association between DEPs and these disorders. They have shown that DEPs upregulate both proinflammatory mediators and antioxidant enzymes in host cells, including bronchial epithelial cells (BECs). The imbalance between proinflammatory mediators and antioxidant proteins may be important to whether DEPs are harmful. Recent progress in this field of research strongly suggests that DEPs can work as potent activators of transcription factors. This effect of DEPs may provide a molecular basis for establishing restriction of diesel motor vehicles as a rational environmental control measure. The present review describes recent research demonstrating the effects of DEPs on BECs.
Purpose of Review: It has been demonstrated that particulate air pollutants such as diesel exhaust particles (DEPs) are associated with allergic respiratory disorders, including asthma and allergic rhinitis. Recent in-vivo and in-vitro studies strongly suggest that DEPs induce both anti-inflammatory and proinflammatory products by activating their transcription. If pollutants are to be controlled in the environment in a cost-effective manner, it is important that the molecular target(s) of DEP-induced responses be elucidated. Bronchial epithelial cells are the key regulators of airway inflammation, and therefore it is crucial to clarify the cellular and molecular mechanisms that are active in these cells. It is also important to compare responses to DEP exposure between healthy and susceptible populations.
Recent Findings: Studies have shown that DEPs activate several signalling pathways such as mitogen-activated protein kinases and transcription factors, in particular nuclear factor-μ and activator protein-1, in human bronchial epithelial cells; these effects are thought to occur via production of reactive oxygen species. Antioxidants effectively reduce the allergic inflammatory effects of DEPs both in vitro and in mice.
Summary: Host responses to DEPs are regulated by a balance between antioxidants and proinflammatory responses. DEP-induced oxidants play a key role in proinflammatory reactions. Recent human studies suggest that chemoprevention against DEP-induced adverse effects in susceptible individuals is possible.
The prevalence of asthma has been increasing in most industrialized countries of the world. Persistent exposure to particulate air pollution from motor vehicles has been implicated as one of the factors that are responsible for the increased prevalence of allergic diseases. Because diesel exhaust particles (DEPs) are the major component of ambient fine particulate matter [i.e. particulate matter of diameter <2.5 µm (PM2.5)], especially in urban areas, many in-vivo and in-vitro studies have been performed to clarify the association between DEPs and these disorders. They have shown that DEPs upregulate both proinflammatory mediators and antioxidant enzymes in host cells, including bronchial epithelial cells (BECs). The imbalance between proinflammatory mediators and antioxidant proteins may be important to whether DEPs are harmful. Recent progress in this field of research strongly suggests that DEPs can work as potent activators of transcription factors. This effect of DEPs may provide a molecular basis for establishing restriction of diesel motor vehicles as a rational environmental control measure. The present review describes recent research demonstrating the effects of DEPs on BECs.
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