Cell reports · 2024
A stress sensor, IRE1α, is required for bacterial-exotoxin-induced interleukin-1β production in tissue-resident macrophages.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Sasaki Izumi, Fukuda-Ohta Yuri, Nakai Chihiro, Wakaki-Nishiyama Naoko, Okamoto Chizuyo, Okuzaki Daisuke, Morita Shuhei, Kaji Shiori, Furuta Yuki, Hemmi Hiroaki, Kato Takashi, Yamamoto Asumi, Tosuji Emi, Saitoh Shin-Ichiroh, Tanaka Takashi, Hoshino Katsuaki, Fukuda Shinji, Miyake Kensuke, Kuroda Etsushi, Ishii Ken J, Iwawaki Takao, Furukawa Koichi, Kaisho Tsuneyasu
Аннотация
Cholera toxin (CT), a bacterial exotoxin composed of one A subunit (CTA) and five B subunits (CTB), functions as an immune adjuvant. CTB can induce production of interleukin-1β (IL-1β), a proinflammatory cytokine, in synergy with a lipopolysaccharide (LPS), from resident peritoneal macrophages (RPMs) through the pyrin and NLRP3 inflammasomes. However, how CTB or CT activates these inflammasomes in the macrophages has been unclear. Here, we clarify the roles of inositol-requiring enzyme 1 alpha (IRE1α), an endoplasmic reticulum (ER) stress sensor, in CT-induced IL-1β production in RPMs. In RPMs, CTB is incorporated into the ER and induces ER stress responses, depending on GM1, a cell membrane ganglioside. IRE1α-deficient RPMs show a significant impairment of CT- or CTB-induced IL-1β production, indicating that IRE1α is required for CT- or CTB-induced IL-1β production in RPMs. This study demonstrates the critical roles of IRE1α in activation of both NLRP3 and pyrin inflammasomes in tissue-resident macrophages.