Inflammasome, IL-1 and inflammation in ozone-induced lung injury - PubMed (original) (raw)

Review

. 2016 Mar 23;5(1):33-40.

eCollection 2016.

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Review

Inflammasome, IL-1 and inflammation in ozone-induced lung injury

Chloé Michaudel et al. Am J Clin Exp Immunol. 2016.

Abstract

Exposure to ambient ozone causes airway hyperreactivity and lung inflammation, which represent an important health concern in humans. Recent clinical and experimental studies contributed to the understanding of the mechanisms of epithelial injury, inflammation and airway hyperreactivity, which is reviewed here. The present data suggest that ozone induced oxidative stress causes inflammasome activation with the release of IL-1, other cytokines and proteases driving lung inflammation leading to the destruction of alveolar epithelia with emphysema and respiratory failure. Insights in the pathogenic pathway may allow to identify novel biomarkers of ozone-induced lung disease and therapeutic targets.

Keywords: DAMP; IL-1; IL-17; NLRP3 inflammasome; ROS; airway hyperreactivity.

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Figures

Figure 1

Figure 1

Mechanism of inflammasome activation. Pollutants, nanoparticles and allergens cause epithelial injury with loss of the epithelial integrity and release of endogenous DAMPs such as HMGB1, UA, ATP and others, leading to inflammasome activation and IL-1β secretion.

Figure 2

Figure 2

Mechanism of ozone-induced injury, hyperreactivity and inflammation. Ozone generates ROS which damage the lung epithelial cells, activating the innate immune response notably the NLRP3 inflammasome with release of IL-1β. Ozone causes increased permeability by down regulating tight junctions and release of alarmins which are released upon cell necrosis. These events induce chemokines/cytokines production and neutrophils recruitment and inflammation.

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