Mannose‐binding lectin as part of the complement pathway: characterization in non‐inflamed and inflamed human eyes

A bstract Background:  Mannose‐binding lectin plays a central effector role in the lectin pathway of complement activation. Frequently occurring MBL2 polymorphisms result in mannose‐binding lectin deficiency, which increases susceptibility to infection. We characterized mannose‐binding lectin levels and function in non‐inflamed and inflamed human eyes, and evaluated its relationship to blood mannose‐binding lectin levels and function. Design:  Prospective, observational clinical study with controls and cases. Participants:  Twenty‐seven patients with paired blood and ocular samples (aqueous and/or vitreous) including 15 controls (non‐inflamed) and 12 cases (inflamed). Methods:  Blood and ocular samples were collected from controls ( n  = 15) with quiet eyes during elective cataract surgery and cases with inflamed eyes including proven/suspected endophthalmitis ( n  = 11) and herpetic retinal vasculitis ( n  = 1). Mannan‐binding and C4 deposition enzyme‐linked quantify mannose‐binding lectin levels and function. Main Outcome Measures:  Blood and ocular mannose‐binding lectin levels and function. Results:  Of 27 patients, 10 (37%) were mannose‐binding lectin‐deficient (defined as blood mannose‐binding lectin levels <500 ng/mL). Blood mannose‐binding lectin levels ( P = 0.16) or function ( P = 0.43) were not significantly different between controls and cases. As expected, there was a high correlation between blood mannose‐binding lectin levels and function (r 2 = 0.74). However, there was significantly more mannose‐binding lectin in inflamed eyes than non‐inflamed eyes measured as level ( P < 0.01) or C4 deposition function ( P < 0.01). Conclusions:  Our study demonstrated that mannose‐binding lectin is significantly elevated in inflamed human eyes but virtually undetectable in non‐inflamed control eyes, suggesting a role in sight‐threatening ocular inflammation.