Contribution of Leukocidin ED to the Pathogenesis of Staphylococcus aureus Endophthalmitis

To test the hypothesis that leukocidin ED (LukED) contributes to the pathogenesis of experimental Staphylococcus aureus endophthalmitis.

Growth curves were generated for S. aureus strain JE2 and strain JE2 lukE::Tn, the transposon mutant of LukED, in brain heart infusion (BHI) and explanted rabbit vitreous. The expression of leukotoxins (lukSF-PV, lukED, hlgABC, and lukGH) was assessed in 18-hour overnight cultures in BHI, tryptic soy broth, and vitreous. S. aureus endophthalmitis was induced by intravitreal injection of 5000 colony-forming units of JE2 or JE2 lukE::Tn into C57BL/6J mice. At 6, 12, and 24 hours after infection, eyes were assessed for retinal function, intraocular colony-forming units and inflammation, and neutrophil infiltration by flow cytometry. RNA was isolated from infected eyes to assess leukotoxin expression.

Strains JE2 and JE2 lukE::Tn grew similarly in BHI and vitreous. Transcript levels of leukotoxin subunits were lower in vitreous compared with laboratory media. In vivo, no differences in retinal function, intraocular growth, intraocular inflation, or neutrophil infiltration were observed in eyes infected with JE2 or JE2 lukE::Tn. During infection, other leukotoxins were expressed in vivo in the absence of LukED.

LukED does not seem to be essential for the pathogenesis of experimental S. aureus endophthalmitis. However, other leukotoxins are expressed in vivo, which may compensate for the effects of LukED during infection.