Abstract：
The pathogenesis of immunoinflammatory rheumatic diseases (IRDs) is based on chronic inflammation, one of the key mechanisms of which may be abnormal activation of macrophages, leading to further disruption of the immune system.
OBJECTIVE: . The objective of this study was to evaluate the proinflammatory activation of circulating monocytes in patients with IRDs.
METHODS: . The study involved 149 participants (53 patients with rheumatoid arthritis (RA), 45 patients with systemic lupus erythematosus (SLE), 34 patients with systemic scleroderma (SSc), and 17 participants without IRDs) 30 to 65 years old. Basal and lipopolysaccharide (LPS)-stimulated secretion of monocytes was studied in a primary culture of monocytes obtained from blood by immunomagnetic separation. Quantitative assessment of the cytokines tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), as well as the chemokine monocyte chemoattractant protein-1 (MCP-1) was carried out in the culture fluid by ELISA. Proinflammatory activation of monocytes was calculated as the ratio of LPS-stimulated and basal secretions.
RESULTS: . It was shown that the basal secretion of all studied cytokines was significantly increased in all groups of patients with IRDs, except for the secretion of IL-1β in the SLE group, compared to the control. LPS-stimulated secretion of TNF-α was increased and MCP-1 was decreased in patients with IRDs compared to the control group; LPS-stimulated IL-1β secretion only in the SSc group significantly differed from the control group. In the RA group, monocyte activation was reduced for all cytokines compared to the control; in the SLE group, for TNF-α and MCP-1; in the SSc group, for MCP-1.
CONCLUSIONS: . The decrease in proinflammatory activation of monocytes in patients with IRDs is due to a high level of basal secretion of cytokines, which can lead to disruption of the adequate immune response in these diseases and is an important link in the pathogenesis of chronic inflammation.
OBJECTIVE: . The objective of this study was to evaluate the proinflammatory activation of circulating monocytes in patients with IRDs.
METHODS: . The study involved 149 participants (53 patients with rheumatoid arthritis (RA), 45 patients with systemic lupus erythematosus (SLE), 34 patients with systemic scleroderma (SSc), and 17 participants without IRDs) 30 to 65 years old. Basal and lipopolysaccharide (LPS)-stimulated secretion of monocytes was studied in a primary culture of monocytes obtained from blood by immunomagnetic separation. Quantitative assessment of the cytokines tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), as well as the chemokine monocyte chemoattractant protein-1 (MCP-1) was carried out in the culture fluid by ELISA. Proinflammatory activation of monocytes was calculated as the ratio of LPS-stimulated and basal secretions.
RESULTS: . It was shown that the basal secretion of all studied cytokines was significantly increased in all groups of patients with IRDs, except for the secretion of IL-1β in the SLE group, compared to the control. LPS-stimulated secretion of TNF-α was increased and MCP-1 was decreased in patients with IRDs compared to the control group; LPS-stimulated IL-1β secretion only in the SSc group significantly differed from the control group. In the RA group, monocyte activation was reduced for all cytokines compared to the control; in the SLE group, for TNF-α and MCP-1; in the SSc group, for MCP-1.
CONCLUSIONS: . The decrease in proinflammatory activation of monocytes in patients with IRDs is due to a high level of basal secretion of cytokines, which can lead to disruption of the adequate immune response in these diseases and is an important link in the pathogenesis of chronic inflammation.
摘要：
免疫炎性风湿性疾病(IRD)的发病机制是以慢性炎症为基础的,其关键机制之一可能是巨噬细胞的异常激活，导致免疫系统的进一步破坏。
目的：。这项研究的目的是评估IRD患者循环单核细胞的促炎激活。
方法：。该研究涉及149名参与者(53名类风湿关节炎(RA)患者，45例系统性红斑狼疮(SLE),34例系统性硬皮病（SSc），和17名没有IRD的参与者）30至65岁。在通过免疫磁性分离从血液中获得的单核细胞的原代培养物中研究了基底和脂多糖（LPS）刺激的单核细胞分泌。细胞因子肿瘤坏死因子α（TNF-α）的定量评估，白细胞介素1β（IL-1β），以及通过ELISA在培养液中进行趋化因子单核细胞趋化蛋白-1(MCP-1)。单核细胞的促炎激活被计算为LPS刺激的和基础分泌物的比率。
结果：。结果表明，在所有IRD患者组中，所有研究的细胞因子的基础分泌均显着增加，SLE组除分泌IL-1β外,与对照相比。与对照组相比，IRD患者LPS刺激的TNF-α分泌增加，MCP-1减少；仅SSc组的LPS刺激的IL-1β分泌与对照组明显不同。在RA组中，与对照组相比，所有细胞因子的单核细胞活化均降低；在SLE组中，对于TNF-α和MCP-1；在SSc组中，对于MCP-1。
结论：。IRD患者单核细胞促炎激活的减少是由于细胞因子的基础分泌水平高，这可能导致这些疾病中足够的免疫反应的破坏，并且是慢性炎症发病机理中的重要环节。
目的：。这项研究的目的是评估IRD患者循环单核细胞的促炎激活。
方法：。该研究涉及149名参与者(53名类风湿关节炎(RA)患者，45例系统性红斑狼疮(SLE),34例系统性硬皮病（SSc），和17名没有IRD的参与者）30至65岁。在通过免疫磁性分离从血液中获得的单核细胞的原代培养物中研究了基底和脂多糖（LPS）刺激的单核细胞分泌。细胞因子肿瘤坏死因子α（TNF-α）的定量评估，白细胞介素1β（IL-1β），以及通过ELISA在培养液中进行趋化因子单核细胞趋化蛋白-1(MCP-1)。单核细胞的促炎激活被计算为LPS刺激的和基础分泌物的比率。
结果：。结果表明，在所有IRD患者组中，所有研究的细胞因子的基础分泌均显着增加，SLE组除分泌IL-1β外,与对照相比。与对照组相比，IRD患者LPS刺激的TNF-α分泌增加，MCP-1减少；仅SSc组的LPS刺激的IL-1β分泌与对照组明显不同。在RA组中，与对照组相比，所有细胞因子的单核细胞活化均降低；在SLE组中，对于TNF-α和MCP-1；在SSc组中，对于MCP-1。
结论：。IRD患者单核细胞促炎激活的减少是由于细胞因子的基础分泌水平高，这可能导致这些疾病中足够的免疫反应的破坏，并且是慢性炎症发病机理中的重要环节。
