PM 2.5 collected in China causes inflammatory and oxidative stress responses in macrophages through the multiple pathways

Bekki, Kanae; Ito, Tomohiro; Yoshida, Yasuhiro; He, Can; Arashidani, Keiichi; He, Miao; Sun, Guifan; Zhou, Yang; Sone, Hirohito; Kunugita, Naoki; Ichinose, Takamichi

doi:10.1016/j.etap.2016.06.022

Cited by 103 publications

(61 citation statements)

References 25 publications

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“…Thus, the effects of NAC in mice lungs were consistent with the effects on the alveolar cell line, but inconsistent with the effects on the macrophage cell lines. We have reported that NAC exhibited no effect on the suppression of PM2.5‐induced proinflammatory responses in RAW264.7 cells (Bekki et al ., ). However, it has been reported that NAC prevented airborne PM1 (<1 μm)‐induced intercellular ROS generation and autophagy in the mouse alveolar cell line MLE‐12 cells (Bai et al ., ).…”

Section: Discussionmentioning

confidence: 97%

PM2.5-induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells

et al. 2017

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Section: Discussionmentioning

confidence: 97%

PM2.5-induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells

et al. 2017

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“…IL-1β production from effected cells has been found in many kinds of lung inflammatory reactions induced by viruses, bacteria and drugs1314. Some in vitro studies found that PM 2.5 could induce the secretion of IL-1β from macrophags through multiple pathways15. The activated TLR4/MyD88/NF-κB pathway participates in the expression of pro-IL-1β in the cytoplasm161718.…”

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confidence: 99%

The acute airway inflammation induced by PM2.5 exposure and the treatment of essential oils in Balb/c mice

Wang

Song

et al. 2017

Sci Rep

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PM2.5 is the main particulate air pollutant whose aerodynamic diameter is less than 2.5 micron. The inflammation of various respiratory diseases are associated with PM2.5 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 PM2.5 related diseases. To elucidate the underlying mechanism of PM2.5-induced acute lung inflammation, we exposed Balb/c mice to PM2.5 intratracheally and established a mice model. Acute lung inflammation and increased IL-1β expression was observed after PM2.5 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 PM2.5-induced acute lung inflammation. The decreased IL-1β and Th immune responses after CEOs treatment were significant. PM2.5 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 PM2.5-induced acute lung inflammation and that may bring about novel therapies for the inflammatory diseases associated with PM2.5 inhalation.

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“…Este puede participar en la reacción de Haber-Weiss formando radicales hidroxilo. La formación de especies reactivas del oxígeno podría explicar en parte el aumento de F 2 isoprostano plasmático, además el PM ultrafino activa a la MAP kinasa (MAPK) por especies reactivas del oxígeno en células endoteliales estimulándose la producción de IL-6 11,34 .…”

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Efecto del sulfato de cobre en el daño pulmonar inducido por la exposición crónica intermitente a ozono

et al. 2017

Rev. méd. Chile

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Effect of copper sulphate on the lung damage induced by chronic intermittent exposure to ozone count, proteins, GGT and AP in BALF (p < 0.05). Foamy and pigmented alveolar macrophages were detected in all lungs of these animals (p < 0.001). Conclusions: Intratracheal instillation of a single dose of CuSO 4 in rats previously subjected to a chronic and intermittent exposure to ozone induces a neutrophil pulmonary inflammatory response and cytoplasmic damage in macrophages. (Rev Med Chile 2017; 145: 9-16)

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PM 2.5 collected in China causes inflammatory and oxidative stress responses in macrophages through the multiple pathways

Cited by 103 publications

References 25 publications

PM2.5-induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells

PM2.5-induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells

The acute airway inflammation induced by PM2.5 exposure and the treatment of essential oils in Balb/c mice

Efecto del sulfato de cobre en el daño pulmonar inducido por la exposición crónica intermitente a ozono

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