7月19日,，Science在線報道,，TLR13受體可識別一類保守的23S核糖體RNA序列,，以及一種圍繞該相互作用的細菌耐藥機制,。
保護宿主免受感染的機制依賴于識別受體,，如Toll樣受體（TLRs）,，以與生俱來的模式識別病原體。
本研究證實,，在小鼠體內(nèi),，孤兒受體TLR13識別一個細菌內(nèi)保守的23S核糖體RNA（rRNA）序列。該序列是大環(huán)內(nèi)酯類,，林肯酰胺以及鏈霉殺陽菌素類（MLS）抗生素（包括紅霉素）的結(jié)合位點,。
值得注意的是，源自從臨床分離的耐紅霉素金黃色葡萄球菌的23S rRNA和帶甲基化腺苷或鳥苷的合成寡核苷酸可模擬導致 MLS抵抗的修飾,。此修飾的結(jié)果是不能激活TLR13,。
總之，該研究結(jié)果發(fā)現(xiàn)了一個天然TLR13配體,，以及一種引發(fā)抗生素耐藥性的具體機制,。該機制通過避免TLR13介導的識別，作為細菌強有力的免疫逃避策略,。（生物谷bioon.com）
doi:10.1016/j.cell.2011.10.017
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PMID:
TLR13 Recognizes Bacterial 23S rRNA Devoid of Erythromycin Resistance–Forming Modification
Marina Oldenburg1,*,Anne Krüger1,*,Ruth Ferstl2,*,?,Andreas Kaufmann3,Gernot Nees3,Anna Sigmund1,Barbara Bathke4,Henning Lauterbach4,Mark Suter4,5,Stefan Dreher2,Uwe Koedel6,Shizuo Akira7,Taro Kawai7,Jan Buer1,Hermann Wagner2,Stefan Bauer3,Hubertus Hochrein4,*,Carsten J. Kirschning
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 S. aureus and synthetic oligoribonucleotides carrying methylated adenosine or a guanosine mimicking a MLS resistance–causing modification failed to stimulate TLR13. Our results thus reveal both a natural TLR13 ligand and specific mechanisms of antibiotic resistance as potent bacterial immune evasion strategy, avoiding recognition via TLR13.
