The virulome in endophthalmitis.

is recognized as a causative agent of gastrointestinal syndromes, but can also cause a devastating form of intraocular infection known as endophthalmitis. We have previously reported that the PlcR/PapR master virulence factor regulator system regulates intraocular virulence, and that the S-layer protein (SlpA) contributes to the severity of endophthalmitis. To better understand the role of other virulence genes in endophthalmitis, expression of a subset of factors was measured at the midpoint of disease progression in a murine model of endophthalmitis by RNA-Seq. Several cytolytic toxins were expressed at significantly higher levels than in BHI. The virulence regulators , , and were also expressed . However, at this timepoint, / was not detectable, although we previously reported that a mutant deficient in PlcR was attenuated in the eye. The motility-related genes , , and , and the chemotaxis-related gene were detected during infection. We have shown previously that motility and chemotaxis phenotypes are important in endophthalmitis. The variant of manganese superoxide dismutase was the most highly expressed gene . Expression of the surface layer protein gene, , an activator of Toll-like receptors (TLR)-2 and -4, was also detected during infection, albeit at low levels. Genes expressed in a mouse model of endophthalmitis might play crucial roles in the unique virulence of endophthalmitis, and serve as candidates for novel therapies designed to attenuate the severity of this often blinding infection.