The acute airway inflammation induced by PM 2.5 exposure and the treatment of essential oils in Balb/c mice
PM is the main particulate air pollutant whose aerodynamic diameter is less than 2.5 micron. The inflammation of various respiratory diseases are associated with PM inhalation. Pro-inflammatory cytokine IL-1β generated from effected cells usually plays a crucial role in many kinds of lung inflammato...
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Veröffentlicht in: | Scientific reports 2017-03, Vol.7, p.44256 |
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Sprache: | eng |
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Zusammenfassung: | PM
is the main particulate air pollutant whose aerodynamic diameter is less than 2.5 micron. The inflammation of various respiratory diseases are associated with PM
inhalation. Pro-inflammatory cytokine IL-1β generated from effected cells usually plays a crucial role in many kinds of lung inflammatory reactions. The exacerbation of Th immune responses are identified in some PM
related diseases. To elucidate the underlying mechanism of PM
-induced acute lung inflammation, we exposed Balb/c mice to PM
intratracheally and established a mice model. Acute lung inflammation and increased IL-1β expression was observed after PM
instillation. Regulatory factors of IL-1β (TLR4/MyD88 signaling pathway and NLRP3 inflammasome) participated in this lung inflammatory response as well. Treatment with compound essential oils (CEOs) substantially attenuated PM
-induced acute lung inflammation. The decreased IL-1β and Th immune responses after CEOs treatment were significant. PM
may increase the secretion of IL-1β through TLR4/MyD88 and NLRP3 pathway resulting in murine airway inflammation. CEOs could attenuate the lung inflammation by reducing IL-1β and Th immune responses in this model. This study describes a potentially important mechanism of PM
-induced acute lung inflammation and that may bring about novel therapies for the inflammatory diseases associated with PM
inhalation. |
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ISSN: | 2045-2322 |
DOI: | 10.1038/srep44256 |