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Serum granulocyte-macrophage colony-stimulating factor (GM-CSF) is increased in patients with active radiographic axial spondyloarthritis and persists despite anti-TNF treatment
Arthritis Research & Therapy ( IF 4.9 ) Pub Date : 2022-08-16 , DOI: 10.1186/s13075-022-02888-6 Charalampos Papagoras 1 , Styliani Tsiami 2 , Akrivi Chrysanthopoulou 3 , Ioannis Mitroulis 1 , Xenofon Baraliakos 2
Arthritis Research & Therapy ( IF 4.9 ) Pub Date : 2022-08-16 , DOI: 10.1186/s13075-022-02888-6 Charalampos Papagoras 1 , Styliani Tsiami 2 , Akrivi Chrysanthopoulou 3 , Ioannis Mitroulis 1 , Xenofon Baraliakos 2
Affiliation
Accumulating evidence supports the role of monocytes and neutrophils in radiographic axSpA (r-axSpA). Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a growth factor for both leukocyte lineages and a pro-inflammatory cytokine activating myeloid cells and promoting osteoclastogenesis. It acts through the JAK-STAT pathway. We measured serum GM-CSF and markers of bone metabolism in patients with r-axSpA before and after anti-TNF treatment. Patients with active r-axSpA despite treatment with NSAIDs, all eligible for treatment with a biologic agent, were recruited. Healthy donors were sampled as controls. Serum was collected before (baseline) and after 4–6 months (follow-up) of anti-TNF treatment and the following molecules were measured with ELISA: GM-CSF, sclerostin (SOST), and dickkopf-1 (Dkk-1). Twelve r-axSpA patients (7 males, 5 females, median age 37 years) with a median disease duration of 1 year and 16 age- and sex-matched controls were included. At baseline, patients had mean BASDAI 6.3±2 and ASDAS 3.2±0.7, which decreased to 4.1±1.7 and 2.2±0.6 at follow-up, respectively. At baseline, r-axSpA patients had significantly higher mean serum levels of GM-CSF (150 vs 62pg/ml, p=0.049), significantly lower Dkk-1 (1228 vs 3052pg/ml, p=0.001), but similar levels of SOST (369 vs 544pg/ml, p=0.144) compared to controls. Anti-TNF treatment did not affect GM-CSF, Dkk-1, or SOST levels. Spearman correlation analysis showed that GM-CSF correlated positively with ASDAS at baseline (r=0.61, p=0.039), while no correlations were identified between bone markers (Dkk-1, SOST) on one hand and GM-CSF or disease activity indices on the other. GM-CSF is increased in patients with active AS and strongly correlates with disease activity. TNF inhibition does not affect GM-SCF levels, despite improving disease activity. GM-CSF may represent an important pathway responsible for residual inflammation during TNF blockade, but also a potential target of JAK inhibitors, explaining their efficacy in r-axSpA.
中文翻译:
活动性中轴型脊柱关节炎患者的血清粒细胞-巨噬细胞集落刺激因子 (GM-CSF) 升高,并且尽管抗 TNF 治疗仍持续存在
越来越多的证据支持单核细胞和中性粒细胞在放射学 axSpA (r-axSpA) 中的作用。粒细胞-巨噬细胞集落刺激因子 (GM-CSF) 是白细胞谱系的生长因子,也是激活骨髓细胞和促进破骨细胞生成的促炎细胞因子。它通过 JAK-STAT 途径起作用。我们在抗 TNF 治疗前后测量了 r-axSpA 患者的血清 GM-CSF 和骨代谢标志物。招募了尽管接受了 NSAIDs 治疗但仍存在活动性 r-axSpA 的患者,这些患者都符合接受生物制剂治疗的条件。健康供体被取样作为对照。在抗 TNF 治疗之前(基线)和 4-6 个月(随访)之后收集血清,并用 ELISA 测量以下分子:GM-CSF、硬化素 (SOST) 和 dickkopf-1 (Dkk-1) . 12 名 r-axSpA 患者(7 名男性,包括 5 名女性,中位年龄 37 岁),中位病程为 1 年和 16 名年龄和性别匹配的对照。基线时,患者的平均 BASDAI 为 6.3±2 和 ASDAS 为 3.2±0.7,随访时分别降至 4.1±1.7 和 2.2±0.6。在基线时,r-axSpA 患者的 GM-CSF 平均血清水平显着升高(150 对 62pg/ml,p=0.049),Dkk-1 显着降低(1228 对 3052pg/ml,p=0.001),但与对照相比,SOST(369 对 544pg/ml,p=0.144)。抗 TNF 治疗不影响 GM-CSF、Dkk-1 或 SOST 水平。Spearman 相关分析显示,GM-CSF 与基线时的 ASDAS 呈正相关(r=0.61,p=0.039),而骨标志物(Dkk-1,SOST)与 GM-CSF 或疾病活动指数之间没有相关性。在另一。活动性 AS 患者的 GM-CSF 升高,并且与疾病活动度密切相关。尽管可以改善疾病活动,但 TNF 抑制并不影响 GM-SCF 水平。GM-CSF 可能代表在 TNF 阻断期间导致残留炎症的重要途径,但也是 JAK 抑制剂的潜在靶标,解释了它们在 r-axSpA 中的功效。
更新日期:2022-08-16
中文翻译:
活动性中轴型脊柱关节炎患者的血清粒细胞-巨噬细胞集落刺激因子 (GM-CSF) 升高,并且尽管抗 TNF 治疗仍持续存在
越来越多的证据支持单核细胞和中性粒细胞在放射学 axSpA (r-axSpA) 中的作用。粒细胞-巨噬细胞集落刺激因子 (GM-CSF) 是白细胞谱系的生长因子,也是激活骨髓细胞和促进破骨细胞生成的促炎细胞因子。它通过 JAK-STAT 途径起作用。我们在抗 TNF 治疗前后测量了 r-axSpA 患者的血清 GM-CSF 和骨代谢标志物。招募了尽管接受了 NSAIDs 治疗但仍存在活动性 r-axSpA 的患者,这些患者都符合接受生物制剂治疗的条件。健康供体被取样作为对照。在抗 TNF 治疗之前(基线)和 4-6 个月(随访)之后收集血清,并用 ELISA 测量以下分子:GM-CSF、硬化素 (SOST) 和 dickkopf-1 (Dkk-1) . 12 名 r-axSpA 患者(7 名男性,包括 5 名女性,中位年龄 37 岁),中位病程为 1 年和 16 名年龄和性别匹配的对照。基线时,患者的平均 BASDAI 为 6.3±2 和 ASDAS 为 3.2±0.7,随访时分别降至 4.1±1.7 和 2.2±0.6。在基线时,r-axSpA 患者的 GM-CSF 平均血清水平显着升高(150 对 62pg/ml,p=0.049),Dkk-1 显着降低(1228 对 3052pg/ml,p=0.001),但与对照相比,SOST(369 对 544pg/ml,p=0.144)。抗 TNF 治疗不影响 GM-CSF、Dkk-1 或 SOST 水平。Spearman 相关分析显示,GM-CSF 与基线时的 ASDAS 呈正相关(r=0.61,p=0.039),而骨标志物(Dkk-1,SOST)与 GM-CSF 或疾病活动指数之间没有相关性。在另一。活动性 AS 患者的 GM-CSF 升高,并且与疾病活动度密切相关。尽管可以改善疾病活动,但 TNF 抑制并不影响 GM-SCF 水平。GM-CSF 可能代表在 TNF 阻断期间导致残留炎症的重要途径,但也是 JAK 抑制剂的潜在靶标,解释了它们在 r-axSpA 中的功效。