Scholarlink

<p>Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by cartilage destruction, low-grade inflammation, and oxidative stress. Emerging evidence suggests that immunometabolic pathways, particularly the tryptophan–kynurenine axis, may contribute to OA pathogenesis. This study aimed to investigate oxidative stress parameters, inflammatory cytokines, and tryptophan metabolism in patients with OA. In this cross-sectional study, serum levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-alpha (TNF-α), interleukin-36 alpha (IL-36α), neopterin, tryptophan, and kynurenine were measured in patients with OA and healthy controls. The kynurenine/tryptophan (KYN/TRP) ratio was calculated as an indirect marker of indoleamine 2,3-dioxygenase-1 (IDO-1) activity. Statistical comparisons between groups were performed to assess potential associations. Serum MDA and IL-36α levels were significantly higher in the OA group compared with controls (<i>p</i> = 0.013 and<i> p</i> = 0.015, respectively). In contrast, serum tryptophan levels were significantly lower in OA patients (<i>p</i> = 0.025). No statistically significant differences were observed in SOD, CAT, kynurenine, neopterin, tumor necrosis factor-alpha (TNF-α) levels, or the KYN/TRP ratio (<i>p</i> &gt; 0.05). These findings suggest that oxidative stress and IL-36α–mediated inflammatory pathways may play a more prominent role in OA pathogenesis than classical systemic inflammatory markers. Reduced tryptophan levels without significant kynurenine pathway activation indicate limited systemic interferon gamma (IFN-γ)–IDO–mediated immune activation in OA. MDA and IL-36α may represent potential candidate biomarkers for disease monitoring. Larger longitudinal studies are required to confirm these observations.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Oxidative Stress and IL-36α–Mediated Inflammation in Osteoarthritis: Association with Tryptophan–Kynurenine Metabolism

  • 期刊论文

  • 发表日期：

    2026年8月4日

查看全文
  • Yasemin Apak,
  • Merih Akkapulu Kaya,
  • Nil Doğruer Ünal,
  • Özlem Bölgen Çimen,
  • Serap Yalın

摘要

Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by cartilage destruction, low-grade inflammation, and oxidative stress. Emerging evidence suggests that immunometabolic pathways, particularly the tryptophan–kynurenine axis, may contribute to OA pathogenesis. This study aimed to investigate oxidative stress parameters, inflammatory cytokines, and tryptophan metabolism in patients with OA. In this cross-sectional study, serum levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-alpha (TNF-α), interleukin-36 alpha (IL-36α), neopterin, tryptophan, and kynurenine were measured in patients with OA and healthy controls. The kynurenine/tryptophan (KYN/TRP) ratio was calculated as an indirect marker of indoleamine 2,3-dioxygenase-1 (IDO-1) activity. Statistical comparisons between groups were performed to assess potential associations. Serum MDA and IL-36α levels were significantly higher in the OA group compared with controls (p = 0.013 and p = 0.015, respectively). In contrast, serum tryptophan levels were significantly lower in OA patients (p = 0.025). No statistically significant differences were observed in SOD, CAT, kynurenine, neopterin, tumor necrosis factor-alpha (TNF-α) levels, or the KYN/TRP ratio (p > 0.05). These findings suggest that oxidative stress and IL-36α–mediated inflammatory pathways may play a more prominent role in OA pathogenesis than classical systemic inflammatory markers. Reduced tryptophan levels without significant kynurenine pathway activation indicate limited systemic interferon gamma (IFN-γ)–IDO–mediated immune activation in OA. MDA and IL-36α may represent potential candidate biomarkers for disease monitoring. Larger longitudinal studies are required to confirm these observations.