Abstract

Aim: To determine the presence of systemic inflammation and innate immune responsiveness of patients with a history of acute anterior uveitis but no signs of ocular inflammation at the time of recruitment.

Methods: Tumour necrosis factor α (TNF-α) production in response to bacterial lipopolysaccharide (LPS) was studied using whole blood culture assay; levels of TNF-α in culture supernatants, and soluble interleukin 2 receptor (sIL-2R) in serum were determined by chemiluminescent immunoassay (Immulite); monocyte surface expression of CD11b, CD14, and CD16 and the proportion of monocyte subsets CD14^brightCD16⁻ and CD14^dimCD16⁺ were studied with three colour whole blood flow cytometry; and serum C reactive protein (CRP) levels were determined using immunonephelometric high sensitivity CRP assay.

Results: The CRP level (median, interquartile range) was significantly higher in 56 patients with previous uveitis than in 37 controls (1.59 (0.63 to 3.47) μg/ml v 0.81 (0.32 to 2.09) μg/ml; p=0.008). The TNF-α concentration of the culture media per 10⁵ monocytes was significantly higher in the patient group than in the control group in the presence of LPS 10 ng/ml (1473 (1193 to 2024) pg/ml v 1320 (935 to 1555) pg/ml; p=0.012) and LPS 1000 ng/ml (3280 (2709 to 4418) pg/ml v 2910 (2313 to 3358) pg/ml; p=0.011). The background TNF-α release into the culture media was low in both groups. CD14 expression of CD14^brightCD16⁻ monocytes, defined as antibody binding capacity (ABC), was similar for the patients and controls (22 839 (21 038 to 26 020) ABC v 21 657 (19 854 to 25 646) ABC).

Conclusions: Patients with previous acute anterior uveitis show high innate immune responsiveness that may play a part in the development of ocular inflammation.