TLR13 Recognizes Bacterial 23S rRNA Devoid of Erythromycin Resistance-Forming Modification
TLR13 Recognizes Bacterial 23S rRNA Devoid of Erythromycin Resistance-Forming Modification
复制标题
DOI：
10.1126/science.1220363
复制
发表时间：
2012-08-31
期刊：
影响因子：
56.9
通讯作者：
Kirschning, Carsten J.
中科院分区：
文献类型：
--
作者：
Oldenburg, Marina;Krueger, Anne;Kirschning, Carsten J.
宿主对感染的保护依赖于先天模式识别受体（如toll样受体（TLRs））对病原体的识别。在这里，我们发现小鼠孤儿受体TLR13识别了一个保守的23S核糖体RNA （rRNA）序列，该序列是细菌中大环内酯、利可沙胺和链状gramin组（MLS）抗生素（包括红霉素）的结合位点。值得注意的是，临床分离的耐红霉素金黄色葡萄球菌的23S rRNA和合成的携带甲基化腺苷或模拟MLS耐药修饰的鸟苷的低核糖核苷酸未能刺激TLR13。因此，我们的研究结果揭示了天然TLR13配体和抗生素抗性的特定机制是有效的细菌免疫逃避策略，避免通过TLR13识别。
Host protection from infection relies on the recognition of pathogens by innate pattern-recognition receptors such as Toll-like receptors (TLRs). Here, we show that the orphan receptor TLR13 in mice recognizes a conserved 23S ribosomal RNA (rRNA) sequence that is the binding site of macrolide, lincosamide, and streptogramin group (MLS) antibiotics (including erythromycin) in bacteria. Notably, 23S rRNA from clinical isolates of erythromycin-resistant Staphylococcus aureus and synthetic oligoribonucleotides carrying methylated adenosine or a guanosine mimicking a MLS resistance-causing modification failed to stimulate TLR13. Thus, our results reveal both a natural TLR13 ligand and specific mechanisms of antibiotic resistance as potent bacterial immune evasion strategy, avoiding recognition via TLR13.