Abstract
Background Endophthalmitis is an uncommon and serious intraocular infection. Endophthalmitis most commonly follows on from cataract surgery or intravitreal injections. The rate of endophthalmitis has fallen in recent years with improved surgical techniques, and infection control. However, despite all precautions, cases of endophthalmitis continue to present. It is possible that poor intraocular immune function makes some patients susceptible to endophthalmitis. We propose that innate phagocytic function is one determinant of the development of endophthalmitis. In order to investigate this, we measured the innate phagocytic function and P2X7 receptor function acutely and at intervals through convalesence for patients who developed endophthalmitis, and compared it with the function of a published population control group.Methods Patients presented to a tertiary eye hospital emergency department with acute endophthalmitis. Informed consent was obtained, and peripheral blood taken. Innate phagocytosis of ethidium and fluorescent latex beads was then quantified using a validated flow cytometric-method at the Florey Institute. Patients had repeat bloods taken at 1 week and 3 months after recruitment.Results P2X7 receptor function was significantly reduced in the endophthalmitis cohort compared to controls. P2X7 function improved through convalescence as patients recovered from endophthalmitis but did not improve to the level of controls. Phagocytic function was reduced in the endophthalmitis cohort compared to controls at all time points. There was no improvement in phagocytic function observed as patients recovered from endophthalmitis.Conclusions The data from this study showed greatly lowered phagocytic function and P2X7 function in patients who developed endophthalmitis, as compared to population controls. This important finding may allow us to predict susceptibility or guide future therapeutics through enhancement of innate phagocytic function.