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Toll/interleukin-1 receptor (TIR) domains in Toll-like receptors are essential for initiating and propagating the eukaryotic innate immune signaling cascade. Here, we investigate TirS, a  Staphylococcus aureus  TIR mimic that is part of a novel bacterial invasion mechanism. Its ectopic expression in eukaryotic cells inhibited TLR signaling, downregulating the NF-kB pathway through inhibition of TLR2, TLR4, TLR5, and TLR9. Skin lesions induced by the  S .  aureus  knockout  tirS  mutant increased in a mouse model compared with wild-type and restored strains even though the  tirS -mutant and wild-type strains did not differ in bacterial load. TirS also was associated with lower neutrophil and macrophage activity, confirming a central role in virulence attenuation through local inflammatory responses. TirS invariably localizes within the staphylococcal chromosomal cassettes (SCC) containing the  fusC  gene for fusidic acid resistance but not always carrying the  mecA  gene. Of note, sub-inhibitory concentration of fusidic acid increased  tirS  expression. Epidemiological studies identified no link between this effector and clinical presentation but showed a selective advantage with a SCC mec  element with SCC  fusC / tirS . Thus, two key traits determining the success and spread of bacterial infections are linked.

The TIR Homologue Lies near Resistance Genes in Staphylococcus aureus, Coupling Modulation of Virulence and Antimicrobial Susceptibility