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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Functional relevance of NLRP3 inflammasome-mediated interleukin (IL)-1β during acute allergic airway inflammation
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Functional relevance of NLRP3 inflammasome-mediated interleukin (IL)-1β during acute allergic airway inflammation

机译：急性过敏性气道炎症中NLRP3炎性体介导的白介素（IL）-1β的功能相关性

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Summary: Overall asthmatic symptoms can be controlled with diverse therapeutic agents. However, certain symptomatic individuals remain at risk for serious morbidity and mortality, which prompts the identification of novel therapeutic targets and treatment strategies. Thus, using an adjuvant-free T helper type 2 (Th2) murine model, we have deciphered the role of interleukin (IL)-1 signalling during allergic airway inflammation (AAI). Because functional IL-1β depends on inflammasome activation we first studied asthmatic manifestations in specific inflammasome-deficient [NACHT, LRR and PYD domains-containing protein 3 (NLRP3-/-) and apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC-/-)] and IL-1 receptor type 1-/- (IL-1R1-/-) mice on the BALB/c background. To verify the onset of disease we assessed cellular infiltration in the bronchial regions, lung pathology, airway hyperresponsiveness and ovalbumin (OVA)-specific immune responses. In the absence of NLRP3 inflammasome-mediated IL-1β release all symptoms of AAI were reduced, except OVA-specific immunoglobulin levels. To address whether manipulating IL-1 signalling reduced asthmatic development, we administered the IL-1R antagonist anakinra (Kineret?) during critical immunological time-points: sensitization or challenge. Amelioration of asthmatic symptoms was only observed when anakinra was administered during OVA challenge. Our findings indicate that blocking IL-1 signalling could be a potential complementary therapy for allergic airway inflammation.
机译：摘要：总体哮喘症状可通过多种治疗药物控制。但是，某些有症状的个体仍然有发生严重发病和死亡的风险，这促使人们确定新的治疗靶点和治疗策略。因此，使用无佐剂2型T辅助小鼠（Th2），我们已经破译了在过敏性气道炎症（AAI）中白介素（IL）-1信号的作用。由于功能性IL-1β依赖于炎性体的激活，因此我们首先研究了特定的炎性体缺陷型[NACHT，LRR和PYD域包含蛋白3（NLRP3-/-）和凋亡相关斑点蛋白（包含caspase募集域）的哮喘表现（ ASC-/-）]和IL-1受体类型1-/-（IL-1R1-/-）小鼠放在BALB / c背景上。为了验证疾病的发作，我们评估了支气管区域的细胞浸润，肺病理学，气道高反应性和卵清蛋白（OVA）特异性免疫反应。在没有NLRP3炎性体介导的IL-1β释放的情况下，除OVA特异性免疫球蛋白水平外，所有AAI症状均得到减轻。为了解决操纵IL-1信号是否减少哮喘的发展，我们在关键的免疫学时间点（致敏或激发）给予了IL-1R拮抗剂anakinra（Kineret？）。仅当在OVA激发期间施用anakinra时，才观察到哮喘症状的改善。我们的发现表明，阻断IL-1信号传导可能是过敏性气道炎症的潜在补充疗法。

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