Department of Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States.
Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States.
Invest Ophthalmol Vis Sci. 2024 Jun 3;65(6):12. doi: 10.1167/iovs.65.6.12.
To test the hypothesis that (C-C motif) ligand 2 (CCL2) and CCL3 impact retinal function decline and inflammation during Staphylococcus aureus endophthalmitis.
Experimental endophthalmitis was initiated by intravitreal injection of 5000 colony-forming units of S. aureus into the eyes of C57BL/6J, CCL2-/-, or CCL3-/- mice. At 12 and 24 hours post-infection, retinal function, bacterial load, and myeloperoxidase levels were quantified.
During S. aureus endophthalmitis, we observed a significant improvement in retinal function in CCL2-/- mice relative to C57BL/6J mice at 12 hours but not at 24 hours. In CCL3-/- mice, retinal function was significantly improved relative to C57BL/6J mice at 12 and 24 hours. The absence of CCL2 did not alter intraocular S. aureus intraocular concentrations. However, CCL3-/- mice had significantly lower intraocular S. aureus at 12 hours but not at 24 hours. No difference in myeloperoxidase levels was observed between C57BL/6J and CCL2-/- mice at 12 hours. CCL3-/- mice had almost no myeloperoxidase at 12 hours. At 24 hours, increased myeloperoxidase was observed in CCL2-/- and CCL3-/- mice relative to C57BL/6J mice.
Although the absence of CCL2 resulted in improved retinal function retention at 12 hours, CCL3 deficiency resulted in improved retinal function at 12 and 24 hours. CCL3 deficiency, but not CCL2 deficiency, resulted in almost no inflammation at 12 hours. However, at 24 hours, the absence of CCL2 or CCL3 resulted in significantly increased inflammation. These results suggest that, although both CCL2 and CCL3 impact intraocular infection outcomes, CCL3 may have a more significant impact in S. aureus endophthalmitis.
验证假说，即（C 基序）配体 2（CCL2）和 CCL3 影响金黄色葡萄球菌眼内炎期间的视网膜功能下降和炎症。
通过向 C57BL/6J、CCL2-/-或 CCL3-/-小鼠的眼睛中注射 5000 个菌落形成单位的金黄色葡萄球菌，引发实验性眼内炎。在感染后 12 和 24 小时，定量评估视网膜功能、细菌载量和髓过氧化物酶水平。
在金黄色葡萄球菌眼内炎期间，我们观察到 CCL2-/-小鼠的视网膜功能在 12 小时时相对于 C57BL/6J 小鼠显著改善，但在 24 小时时没有改善。在 CCL3-/-小鼠中，视网膜功能在 12 和 24 小时时相对于 C57BL/6J 小鼠显著改善。CCL2 的缺失并未改变眼内金黄色葡萄球菌的浓度。然而，CCL3-/-小鼠在 12 小时时眼内金黄色葡萄球菌浓度显著降低，但在 24 小时时没有差异。在 12 小时时，C57BL/6J 和 CCL2-/-小鼠之间的髓过氧化物酶水平没有差异。CCL3-/-小鼠在 12 小时时几乎没有髓过氧化物酶。在 24 小时时，CCL2-/-和 CCL3-/-小鼠的髓过氧化物酶水平相对于 C57BL/6J 小鼠增加。
尽管 CCL2 的缺失导致 12 小时时视网膜功能保持改善，但 CCL3 的缺乏导致 12 和 24 小时时视网膜功能改善。CCL3 的缺乏，但不是 CCL2 的缺乏，导致 12 小时时几乎没有炎症。然而，在 24 小时时，CCL2 或 CCL3 的缺失导致炎症显著增加。这些结果表明，尽管 CCL2 和 CCL3 都影响眼内感染结局，但 CCL3 在金黄色葡萄球菌眼内炎中可能具有更显著的影响。
