Journal
SCIENCE
Volume 337, Issue 6098, Pages 1111-1115Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1220363
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Funding
- German research foundation (Deutsche Forschungsgemeinschaft) [KI 591/4-1, GK1045, BA 1618/5-1]
- Japanese Government
- Behring Rontgen Stiftung [56-0034]
- Coley Pharmaceuticals/Pfizer
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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.
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