The ATP/P2X7 axis of dendritic cells (DCs) mediates the activation of NLRP3 inflammasome and promotes secretion of interleukin (IL)−1β and IL-18 to induce T helper (Th) 2, Th17 differentiation in the pathogenesis of asthma. NLRP3 inflammasome also regulates high mobility protein 1 (HMGB1) release in DCs. Recent studies demonstrated the correlation between HMGB1 expression and airway inflammation and hyper-responsiveness (AHR) in asthma. However, the relationship between the ATP/P2X7-NLRP3 axis and HMGB1 in DCs in asthma is still unclear. ATP, apyrase, Brilliant Blue G, BzATP, glibenclamide, and Z-YVAD-FMK were administered to ovalbumin (OVA)-induced murine asthmatic model. For in vitro studies, bone marrow-derived mononuclear cells (BMDCs) were primed with LPS and stimulated with the same reagents. Activation of the ATP/P2X7 axis aggravated airway inflammation and AHR in the lung and induced Th2, Th17 polarization in asthmatic mice. Inhibition of NLRP3 inflammasome weakened cardinal features of asthma and blocked Th2, Th17 polarization. In vitro and vivo, ATP/P2X7 axis activated NLRP3 inflammasome and induced HMGB1 expression and release from DCs. Inhibition of NLRP3 inflammasome reduced HMGB1 expression and release. The ATP/P2X7-NLRP3 axis of DCs participates in mediating airway inflammation, AHR, and promoting Th2, Th17 inflammatory responses in asthmatic mice by inducing HMGB1 expression and secretion.

树突状细胞（DC）的ATP / P2X7轴介导NLRP3炎性小体的激活，并促进白介素（IL）-1β和IL-18的分泌，从而在哮喘发病机理中诱导T辅助（Th）2，Th17分化。NLRP3炎性小体还调节DC中高迁移率蛋白1（HMGB1）的释放。最近的研究表明，哮喘患者中HMGB1表达与气道炎症和高反应性（AHR）之间存在相关性。然而，哮喘DC中ATP / P2X7-NLRP3轴与HMGB1之间的关系仍不清楚。对卵清蛋白（OVA）诱导的小鼠哮喘模型施用ATP，双磷酸腺苷三磷酸酶，亮蓝G，BzATP，格列本脲和Z-YVAD-FMK。为了进行体外研究，用LPS灌注骨髓来源的单核细胞（BMDC），并用相同的试剂刺激。ATP / P2X7轴的激活加剧了肺部气道炎症和AHR，并在哮喘小鼠中诱导了Th2，Th17极化。抑制NLRP3炎性体减弱了哮喘的基本特征，并阻断了Th2，Th17极化。在体外和体内，ATP / P2X7轴激活NLRP3炎性小体并诱导HMGB1表达和从DC中释放。NLRP3炎性体的抑制降低了HMGB1的表达和释放。DC的ATP / P2X7-NLRP3轴通过介导HMGB1表达和分泌，参与介导哮喘小鼠的气道炎症，AHR和促进Th2，Th17炎症反应。ATP / P2X7轴激活NLRP3炎性小体并诱导HMGB1表达并从DC中释放。NLRP3炎性体的抑制降低了HMGB1的表达和释放。DC的ATP / P2X7-NLRP3轴通过介导HMGB1表达和分泌，参与介导哮喘小鼠的气道炎症，AHR和促进Th2，Th17炎症反应。ATP / P2X7轴激活NLRP3炎性小体并诱导HMGB1表达并从DC中释放。NLRP3炎性体的抑制降低了HMGB1的表达和释放。DC的ATP / P2X7-NLRP3轴通过介导HMGB1表达和分泌，参与介导哮喘小鼠的气道炎症，AHR和促进Th2，Th17炎症反应。