Pathogens are recognized by hosts using various receptors including the TLR- and NLR-families. Ligands, for these varied receptors including bacterial products, are identified by the immune system resulting in development of innate immune responses. Only a couple of components from type III secretion systems are known to be recognized by TLR or NLR family members. Known T3S component that are detected by PRRs are; 1) flagellin by TLR5 and NLRC4 (Ipaf) and; 2) T3S rod proteins (PrgJ and homologs) and needle proteins (PrgI and homologs) by NAIP and the NLRC4 inflammasome. In this report we characterize the induction of pro-inflammatory responses through TLRs by the Yersinia pestis T3S needle protein, YscF, the Sa... More
Pathogens are recognized by hosts using various receptors including the TLR- and NLR-families. Ligands, for these varied receptors including bacterial products, are identified by the immune system resulting in development of innate immune responses. Only a couple of components from type III secretion systems are known to be recognized by TLR or NLR family members. Known T3S component that are detected by PRRs are; 1) flagellin by TLR5 and NLRC4 (Ipaf) and; 2) T3S rod proteins (PrgJ and homologs) and needle proteins (PrgI and homologs) by NAIP and the NLRC4 inflammasome. In this report we characterize the induction of pro-inflammatory responses through TLRs by the Yersinia pestis T3S needle protein, YscF, the Salmonella enterica needle proteins PrgI and SsaG, and the Shigella needle protein MxiH. More specifically we determine that the pro-inflammatory responses occur through TLRs 2 and 4. This data supports a hypothesis that T3S needles have an unrecognized role in bacterial pathogenesis by modulating immune responses.