title: Acute inflammation and loss of retinal architecture and function during experimental Bacillus endophthalmitis.
abstract: Rapid vision loss and explosive inflammation are devastating consequences of Bacillus endophthalmitis that have not been well defined. We therefore analyzed the evolution of intraocular inflammation and loss of retinal architecture and function during experimental Bacillus endophthalmitis. Mice were intravitreally injected with 100 CFU of B. cereus, and eyes were analyzed for bacterial growth, retinal function, architectural changes and retinal cellular stress, inflammatory cytokines, and infiltrating cells. Retinal electrophysiologic and structural changes began as early as 4 to 6 hr postinfection. Significant declines in retinal function paralleled the loss of retinal architecture. Glial fibrillary acidic protein (GFAP) was detected in retina, indicating potential stress. Polymorphonuclear leukocyte (PMN) infiltration into the vitreous began as early as 4 hr postinfection, coinciding with a significant increase in TNF-alpha in the eye. These results indicated that acute inflammation and detrimental architectural and electrophysiologic changes in the retina began earlier than once thought, suggesting that therapeutic intervention should be given at the earliest possible time to avoid vision loss during Bacillus endophthalmitis.
authors.affiliation: Oklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
authors.forename: Raniyah T
authors.initials: RT
authors.lastname: Ramadan
authors.forename: Raul
authors.initials: R
authors.lastname: Ramirez
authors.forename: Billy D
authors.initials: BD
authors.lastname: Novosad
authors.forename: Michelle C
authors.initials: MC
authors.lastname: Callegan
mesh_terms: D000208:Acute Disease; D000818:Animals; D016863:Bacillaceae Infections / Q000382:microbiology* / Q000473:pathology; D001409:Bacillus cereus / Q000472:pathogenicity*; D004195:Disease Models, Animal; D009877:Endophthalmitis / Q000382:microbiology* / Q000473:pathology; D015818:Eye Infections, Bacterial / Q000382:microbiology* / Q000473:pathology; D005434:Flow Cytometry; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007150:Immunohistochemistry; D007249:Inflammation / Q000382:microbiology / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009504:Neutrophils / Q000502:physiology; D009195:Peroxidase / Q000378:metabolism; D012164:Retinal Diseases / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D005904:Glial Fibrillary Acidic Protein; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase