Inflammasomes in cigarette smoke- or ozone-induced lung diseases

Chronic obstructive pulmonary disease (COPD) is a major health issue not only due to cigarette smoking but also to air pollution, in particular ozone exposure that is expected to increase in the context of global warming. COPD is characterized by progressive airway obstruction and impaired immune response to bacterial and viral infections. Pollutants induce pulmonary damage, chronic inflammation, and mucus hypersecretion leading to bronchial obstruction, alveolar wall destruction, and strongly impairing lung functions. The underlying mechanisms resulting in chronic inflammation, exacerbation, and impaired lung function remain poorly understood. However, oxidative stress and host-derived danger signals are common triggers leading to cigarette smoke (CS)- or ozone-induced lung injury and inflammation notably by activating inflammasome pathways. Inflammasomes are cytoplasmic multiprotein complexes involved in the regulation of homeostasis and inflammation. Their activation leads to maturation and secretion of major proinflammatory cytokines IL-1β and IL-18 as well as gasdermin D-mediated pore formation. Here we review recent studies analyzing the role of the inflammasomes in human and animal models of CS- or ozone-exposure in the development of pulmonary inflammation potentially leading to COPD and/or fibrosis.