Elevated levels of advanced glycation end-products AGE10 in patients with reactive arthritis caused by Chlamydia trachomatis and Epstein-Barr virus infection.

Advanced glycation end products (AGEs), and particularly the unique AGE10 epitope, may be a potential biomarker of immunopathology in rheumatic diseases. They may be associated with inflammation, joint damage and ossification processes. AGE10 present in human and animal tissues could be detected with monoclonal antibody against melibiose-derived glycation product MAGE synthesized in anhydrous conditions. This MAGE product was different from the classic synthesis in water solution. The epitope was determined in serum with ELISA using these anti-MAGE monoclonal antibodies. This work aims to determine serum AGE10 levels in patients with reactive arthritis (ReA)-caused with Chlamydia trachomatis (group 2) and ReA with C. trachomatis during the reactivation of EBV infection (group 3). Additionally, ankylosing spondylitis (AS) patients (group 4) were involved in the study, due to the potential evolution of ReA toward AS. The control group maintained physiological AGE10 levels (316 µg/ml), while the combined infection group showed elevated AGE10 (850 µg/ml) compared to the chlamydial-only group (17 µg/ml). Fluorescent fAGE were at the highest level in AS patients. A striking finding was the complete absence of detectable AGE10 antigen in the AS group, coinciding with notably elevated immune complex AGE10-anti-AGE10 levels. A similar pattern was observed in patients with ReA caused by C. trachomatis alone (Group 2), albeit to a lesser extent. In contrast, both the control group and patients with ReA associated with EBV coinfection (group 3) displayed an inverse relationship, characterized by higher antigen levels and lower immune complex concentrations. Thus, diminished level of AGE10 could be caused, besides local accumulation, also by immune complexes formation, a pathogenic factor. Therefore, evaluating disease activity in ReA and AS is crucial to further our understanding of the pathophysiology of AGEs formation and predicting prognosis.