Abstract
Abstract: :
Purpose: To examine the mechanisms of retinal function loss in Bacillus endophthalmitis, focusing on the contribution of Muller cell dysfunction to pathogenesis. Methods: Pathogenesis of experimental Bacillus endophthalmitis was analyzed by bacterial quantification, electroretinography, and immunohistochemistry of histology sections and retinal wholemounts for lectin and glial fibrillary acidic protein (GFAP). The cytopathic effects of Bacillus growth and toxin production on human Muller cells in vitro were examined by analysis of membrane integrity, viability, and GFAP and inflammatory cytokine expression. Results: In the eye, Bacillus growth increased logarithmically while b–wave function declined precipitously during the first 12 hours of infection. During the course of infection, increased retinal GFAP immunostaining was observed. In addition, lectin staining revealed areas of cellular leakage and vessel engorgement during the later stages of infection. In vitro, Muller cell membrane integrity loss and cell death was dependent upon the infectious dose and time of Bacillus exposure. No significant increases in inflammatory cytokines (TNFα, MIP–1α, IL–1α) were detected, but IL–6 was expressed constitutively by Muller cells in vitro. Conclusions: Taken together, the in vitro and in vivo results indicated that Bacillus can kill Muller cells, and the rapid b–wave function loss coupled with the increasing retinal GFAP immunostaining suggested Muller cell dysfunction during the course of infection. Further analysis of the specific toxin–mediated mechanisms of Muller cell death during Bacillus endophthalmitis is in progress.
Keywords: bacterial disease • endophthalmitis • Muller cells