Functional relevance of NLRP3 inflammasome-mediated interleukin (IL)-1β during acute allergic airway inflammation

摘要: 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 targets treatment strategies. Thus, using an adjuvant-free T helper type 2 (Th2) murine model, we have deciphered role interleukin (IL)-1 signalling during allergic airway inflammation (AAI). Because functional IL-1? depends on inflammasome activation first studied manifestations in specific inflammasome-deficient [NACHT, LRR PYD domains-containing protein 3 (NLRP3(-/-) ) apoptosis-associated speck-like containing a caspase recruitment domain (ASC(-/-) )] IL-1 receptor 1(-/-) (IL-1R1(-/-) mice BALB/c background. To verify onset disease assessed cellular infiltration bronchial regions, lung pathology, hyperresponsiveness ovalbumin (OVA)-specific immune responses. In absence NLRP3 inflammasome-mediated release all AAI were reduced, except OVA-specific immunoglobulin levels. address whether manipulating reduced development, administered IL-1R antagonist anakinra (Kineret®) critical immunological time-points: sensitization or challenge. Amelioration was only observed when OVA Our findings indicate that blocking could potential complementary therapy inflammation.