Adipose tissue (AT) plays a central role in systemic metabolic homeostasis, but its function during bacterial infection remains unclear. Following subcutaneous bacterial infection, adipocytes surrounding draining lymph nodes initiated a transcriptional response indicative of stimulation with IFN-γ and a shift away from lipid metabolism toward an immunologic function. Natural killer (NK) and invariant NK T (iNKT) cells were identified as sources of infection-induced IFN-γ in perinodal AT (PAT). IFN-γ induced Nos2 expression in adipocytes through a process dependent on nuclear-binding oligomerization domain 1 (NOD1) sensing of live intracellular bacteria. iNOS expression was coupled to metabolic rewiring, inducing increased diversion of extracellular L-arginine through the arginosuccinate shunt and urea cycle to produce nitric oxide (NO), directly mediating bacterial clearance. In vivo, control of infection in adipocytes was dependent on adipocyte-intrinsic sensing of IFN-γ and expression of iNOS. Thus, adipocytes are licensed by innate lymphocytes to acquire anti-bacterial functions during infection.

脂肪组织 (AT) 在全身代谢稳态中发挥核心作用，但其在细菌感染期间的功能仍不清楚。皮下细菌感染后，引流淋巴结周围的脂肪细胞启动了转录反应，表明受到 IFN-γ 的刺激，并从脂质代谢转向免疫功能。自然杀伤 (NK) 和不变的 NK T (iNKT) 细胞被确定为围节期 AT (PAT) 中感染诱导的 IFN-γ 的来源。IFN-γ诱导的Nos2通过依赖于活细胞内细菌的核结合寡聚化结构域 1 (NOD1) 感应的过程在脂肪细胞中表达。iNOS 表达与代谢重新布线相结合，通过精氨酸琥珀酸分流和尿素循环诱导细胞外 L-精氨酸的转移增加，从而产生一氧化氮 (NO)，直接介导细菌清除。在体内，脂肪细胞感染的控制依赖于脂肪细胞对 IFN-γ 的内在感知和 iNOS 的表达。因此，脂肪细胞被先天淋巴细胞许可在感染期间获得抗菌功能。