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Cytokine ; 127: 154983, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-31918161

RESUMO

Inflammasome activation induces the maturation and secretion of interleukin (IL)-1ß and -18, and is dependent on NF-κB signaling to induce the transcription of the inflammasome components, called the priming step. This study elucidated the role of IκBζ, an atypical IκBs (inhibitor of κB) and a coactivator of NF-κB target genes, on the activation of inflammasome. Bone marrow-derived macrophages (BMDMs) that originated from IκBζ-encoding Nfkbiz gene depletion mice presented a defect in NLRP3 inflammasome activation. In addition, the Nfkbiz+/- and Nfkbiz-/- mice significantly attenuated serum IL-1ß secretion in response to a monosodium urate injection, a NLRP3 trigger, when compared with Nfkbiz-+/+ mice. The lack of IκBζ in BMDMs produced a disability in the expression of Nlrp3 and pro-Il1ß mRNAs during the priming step. In addition, ectopic IκBζ expression enhanced the Nlrp3 promoter activity, and Nlrp3 and pro-Il1ß transcription. Overall, IκBζ controlled the activation of NLRP3 inflammasome by upregulating the Nlrp3 gene during the priming step.


Assuntos
Proteínas Adaptadoras de Transdução de Sinal/genética , Inflamassomos/genética , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Regulação para Cima/genética , Animais , Células Cultivadas , Macrófagos/metabolismo , Camundongos , Regiões Promotoras Genéticas/genética , Células RAW 264.7 , RNA Mensageiro/genética , Transdução de Sinais/genética , Transcrição Gênica/genética
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