Bacterial cell wall components of Staphylococcus aureus induce endophthalmitis

AIM: To compare the responses of intraocular inflammation induced by heat-inactivated Staphylococcus aureus or its bacterial cell wall components in SD rats. METHODS: The rats were randomly divided into heat-inactivated bacteria (HIB) group (96 rats were injected with 10 μg of HIB), heat-inactivated bacteria fragments (HIBF) group (96 rats were injected with 10 μg of HIBF), peptidoglycan (PGN) group (96 rats were injected with 10 μg of PGN) and control group (96 rats were injected with sterile saline equivalent). At time points of 6 h, 12 h, 24 h, 48 h, 72 h and 5 d after vitreous injection of the pathogens, the ocular inflammation scores were determined under slit lamp microscope. The infiltration of white blood cells were counted in histological sections. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and cytokine induced neutrophil chemoattractant-1 (CINC-1) in serum and vitreous body were detected by ELISA, and protein concentration in aqueous humor were also measured. RESULTS: Severe ocular inflammation was observed in the animals of HIB, HIBF and PGN groups 6-72 h after injection. Five days after injection, the endophthalmitis subsided. The peak of intraocular white blood cell infiltration was observed 24 h after exposure to the bacteria and the components in each group and the cell infiltration rapidly declined after 3 days. The concentrations of TNF-α and IL-1β peaked at 24 h in each group, maintained to 48 h, then decreased rapidly, and returned to baseline level after 5 days. The concentration of CINC-1 peaked at 12 h in each group, and maintained to 24 h, then decreased rapidly, and returned to the normal level after 3 days. Significantly higher protein levels in aqueous humor were detected in the experimental groups at all time points as compared to that in control group (P<0.01). CONCLUSION: Staphylococcus aureus cells and its components induce typical experimental endophthalmitis in SD rats. Massive leukocyte infiltration and high levels of TNF-α, IL-1β and CINC-1 are the main pathological features in the experimental model. PGN and the bacterial cell wall fragments induce stronger intraocular inflammations than the whole heat-inactivated S. aureus.