While MyD88 signaling is protective against a number of pathogens, how MyD88 alters host metabolism to restrict bacterial infection has not been well studied. During Brucella infection, Lacey et al. (e00156-21) find that MyD88 signaling promotes macrophage glycolysis and that MyD88 deficiency results in an increased availability of glucose in vivo, which Brucella can exploit via the glucose transporter, GluP. MyD88 also promoted production of the metabolite itaconate, which in turn had antibacterial and immunomodulatory effects during Brucella infection.

中文翻译：

---

本期重要文章

虽然 MyD88 信号传导对许多病原体具有保护作用，但尚未充分研究 MyD88 如何改变宿主代谢以限制细菌感染。在布鲁氏菌感染期间，Lacey 等人。(e00156-21) 发现 MyD88 信号传导促进巨噬细胞糖酵解，并且 MyD88 缺乏导致体内葡萄糖的可用性增加，布鲁氏菌可以通过葡萄糖转运蛋白 GluP 来利用这一点。MyD88 还促进代谢物衣康酸盐的产生，而衣康酸盐又在布鲁氏菌感染期间具有抗菌和免疫调节作用。