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 24hours 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 12hours but not at 24hours. In CCL3-/- mice, retinal function was significantly improved relative to C57BL/6J mice at 12 and 24hours. The absence of CCL2 did not alter intraocular S. aureus intraocular concentrations. However, CCL3-/- mice had significantly lower intraocular S. aureus at 12hours but not at 24hours. No difference in myeloperoxidase levels was observed between C57BL/6J and CCL2-/- mice at 12hours. CCL3-/- mice had almost no myeloperoxidase at 12hours. At 24hours, 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 12hours, CCL3 deficiency resulted in improved retinal function at 12 and 24hours. CCL3 deficiency, but not CCL2 deficiency, resulted in almost no inflammation at 12hours. However, at 24hours, 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.