Abstract
BackgroundAccumulating evidence has demonstrated a pathogenic role of advanced glycation end products (AGEs) and receptors for AGEs (RAGE) in inflammation. Soluble RAGE (sRAGE), with the same ligands-binding capacity as full-length RAGE, acts as a “decoy” receptor. However, there has been scanty data regarding AGEs and sRAGE in adult-onset Still’s disease (AOSD). This study aimed to investigate AGEs and sRAGE levels in AOSD patients and examine their association with clinical characteristics.MethodsUsing ELISA, plasma levels of AGEs and sRAGE were determined in 52 AOSD patients, 36 systemic lupus erythematosus(SLE) patients and 16 healthy controls(HC). Their associations with activity parameters and disease courses were evaluated.ResultsSignificantly higher median levels of AGEs were observed in active AOSD patients (16.75 pg/ml) and active SLE patients (14.80 pg/ml) than those in HC (9.80 pg/ml, both p < 0.001). AGEs levels were positively correlated with activity scores (r = 0.836, p < 0.001), ferritin levels (r = 0.372, p < 0.05) and CRP levels (r = 0.396, p < 0.005) in AOSD patients. Conversely, significantly lower median levels of sRAGE were observed in active AOSD patients (632.2 pg/ml) and active SLE patients (771.6 pg/ml) compared with HC (1051.7 pg/ml, both p < 0.001). Plasma sRAGE levels were negatively correlated with AOSD activity scores (r = −0.320, p < 0.05). In comparison to AOSD patients with monocyclic pattern, significantly higher AGEs levels were observed in those with polycyclic or chronic articular pattern. With treatment, AGEs levels declined while sRAGE levels increased in parallel with the decrease in disease activity.ConclusionThe elevation of AGEs levels with concomitant decreased sRAGE levels in active AOSD patients, suggests their pathogenic role in AOSD.
Highlights
Accumulating evidence has demonstrated a pathogenic role of advanced glycation end products (AGEs) and receptors for Advanced glycation end products (AGEs) (RAGE) in inflammation
There were no significant differences in age at onset, proportion of females, body mass index (BMI), or proportion of past or present smoker between adult-onset Still’s disease (AOSD) patients and systemic lupus erythematosus (SLE) patients or healthy subjects (Table 1)
In conclusion, increased AGEs as well as decreased Soluble RAGE (sRAGE), which were significantly correlated with disease activity parameters, may be involved in AOSD pathogenesis
Summary
Accumulating evidence has demonstrated a pathogenic role of advanced glycation end products (AGEs) and receptors for AGEs (RAGE) in inflammation. The increased accumulation of AGEs has been shown positively correlated with disease duration in systemic lupus erythematosus (SLE) [5,6,7]. These observations point to a pathogenic role of AGEs in inflammatory diseases. The interaction of AGEs with full-length RAGE induces activation of intracellular signaling and results in secretion of cytokines such as TNF-α, which plays a major role in inflammatory responses [13,14]
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