Targeting NLRP3 Inflammasome Activation in Severe Asthma

摘要: Severe asthma (SA) is a chronic lung disease characterized by recurring symptoms of reversible airflow obstruction, airway hyper-responsiveness (AHR), and inflammation that resistant to currently employed treatments. The nucleotide-binding oligomerization domain-like Receptor Family Pyrin Domain Containing 3 (NLRP3) inflammasome an intracellular sensor detects microbial motifs endogenous danger signals represents key component innate immune responses in the airways. Assembly NLRP3 leads caspase 1-dependent release pro-inflammatory cytokines IL-1β IL-18 as well pyroptosis. Accumulating evidence proposes activation critically involved pathogenesis. In fact, although facilitates clearance pathogens airways, persistent inhaled irritants and/or innocuous environmental allergens can lead overt pulmonary exacerbation manifestations. Notably, administration inhibitors models restrains AHR inflammation. Here, we provide overview pathophysiology SA, present molecular mechanisms underlying aberrant inflammatory summarize recent studies pertinent biology functions NLRP3, discuss role pathogenesis asthma. Finally, contemplate potential targeting novel therapeutic approach for management SA.