Department of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
The University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences, UTHealth Houston, Houston, Texas, USA.
JCI Insight. 2024 Nov 8;9(21):e180584. doi: 10.1172/jci.insight.180584.
Pneumonia is a worldwide threat to public health, demanding novel preventative and therapeutic strategies. The lung epithelium is a critical environmental interface that functions as a physical barrier to pathogen invasion while also actively sensing and responding to pathogens. We have reported that stimulating lung epithelial cells with a combination therapeutic consisting of a diacylated lipopeptide and a synthetic CpG oligodeoxynucleotide (ODN) induces synergistic pneumonia protection against a wide range of pathogens. We report here that mice deficient in TLR9, the previously described receptor for ODN, still displayed partial ODN-induced protection. This prompted us to seek an alternate ODN receptor, and we discovered by mass spectroscopy that the RNA sensor RIG-I could also bind DNA-like ODN. ODN binding by RIG-I resulted in MAVS-dependent pneumonia-protective signaling events. While RIG-I is essential to native defenses against viral infections, we report that therapeutic RIG-I activation with ODN promoted pathogen killing and host survival following both viral and bacterial challenges. These data indicate that maximal ODN-induced pneumonia protection requires activation of both the TLR9/MyD88 and RIG-I/MAVS signaling pathways. These findings not only identify what we believe to be a novel pattern recognition receptor for DNA-like molecules, but reveal a potential therapeutic strategy to protect susceptible individuals against lethal pneumonias during periods of peak vulnerability.
肺炎是全球公共卫生的威胁,需要新的预防和治疗策略。肺上皮细胞是一个关键的环境界面,它作为物理屏障来防止病原体入侵,同时还能主动感知和响应病原体。我们已经报告说,用一种由二酰化脂肽和合成 CpG 寡脱氧核苷酸 (ODN) 组成的联合治疗方法刺激肺上皮细胞,可以诱导针对广泛病原体的协同肺炎保护作用。我们在这里报告说,TLR9 缺失的小鼠,即先前描述的 ODN 受体,仍然显示出部分 ODN 诱导的保护作用。这促使我们寻找替代的 ODN 受体,我们通过质谱法发现 RNA 传感器 RIG-I 也可以结合 DNA 样 ODN。RIG-I 与 ODN 的结合导致依赖 MAVS 的肺炎保护信号事件。虽然 RIG-I 对于天然防御病毒感染是必不可少的,但我们报告说,用 ODN 进行治疗性 RIG-I 激活可以促进病毒和细菌挑战后的病原体杀伤和宿主存活。这些数据表明,最大程度的 ODN 诱导的肺炎保护作用需要激活 TLR9/MyD88 和 RIG-I/MAVS 信号通路。这些发现不仅确定了我们认为是 DNA 样分子的新型模式识别受体,而且还揭示了一种潜在的治疗策略,可以在易受伤害的高峰期保护易感个体免受致命性肺炎的侵害。