Abstract:
: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 SCCmec element with SCC fusC/tirS. Thus, two key traits determining the success and spread of bacterial infections are linked.
journal_name
PLoS Pathogjournal_title
PLoS pathogensauthors
Patot S,Imbert PR,Baude J,Martins Simões P,Campergue JB,Louche A,Nijland R,Bès M,Tristan A,Laurent F,Fischer A,Schrenzel J,Vandenesch F,Salcedo SP,François P,Lina Gdoi
10.1371/journal.ppat.1006092subject
Has Abstractpub_date
2017-01-06 00:00:00pages
e1006092issue
1eissn
1553-7366issn
1553-7374pii
PPATHOGENS-D-16-01375journal_volume
13pub_type
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