Proinflammatory Activation of Monocytes in Patients with Immunoinflammatory Rheumatic Diseases

IF 0.8 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
A. I. Bogatyreva, E. V. Gerasimova, T. V. Kirichenko, Yu. V. Markina, T. V. Popkova, M. V. Shalygina, T. V. Tolstik, A. M. Markin, A. N. Orekhov
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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.

. The objective of this study was to evaluate the proinflammatory activation of circulating monocytes in patients with IRDs.

. 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.

. 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.

. 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.

Abstract Image

Abstract Image

免疫炎症性风湿病患者单核细胞的促炎性激活。
免疫炎症性风湿病(IRDs)的发病机制以慢性炎症为基础,其关键机制之一可能是巨噬细胞的异常激活,从而导致免疫系统的进一步破坏。本研究的目的是评估 IRD 患者循环单核细胞的促炎症激活情况。这项研究涉及 149 名 30 至 65 岁的参与者(53 名类风湿性关节炎(RA)患者、45 名系统性红斑狼疮(SLE)患者、34 名系统性硬皮病(SSc)患者和 17 名无 IRD 患者)。通过免疫磁性分离从血液中获得的单核细胞原代培养物,对单核细胞的基础分泌和脂多糖(LPS)刺激分泌进行了研究。通过 ELISA 方法对培养液中的细胞因子肿瘤坏死因子α(TNF-α)、白细胞介素 1β(IL-1β)以及趋化因子单核细胞趋化蛋白-1(MCP-1)进行了定量评估。以 LPS 刺激分泌物与基础分泌物之比计算单核细胞的促炎活化。结果表明,与对照组相比,除系统性红斑狼疮组 IL-1β 的分泌外,所有研究细胞因子的基础分泌在所有 IRD 患者组中都显著增加。与对照组相比,IRDs 患者在 LPS 刺激下 TNF-α 的分泌增加,MCP-1 的分泌减少;只有 SSc 组在 LPS 刺激下 IL-1β 的分泌与对照组有明显差异。与对照组相比,RA 组单核细胞活化的所有细胞因子均减少;SLE 组单核细胞活化的 TNF-α 和 MCP-1 均减少;SSc 组单核细胞活化的 MCP-1 减少。IRD患者的单核细胞促炎激活减少是由于细胞因子的基础分泌水平较高,这会导致这些疾病的适当免疫反应被破坏,是慢性炎症发病机制中的一个重要环节。
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来源期刊
Doklady Biochemistry and Biophysics
Doklady Biochemistry and Biophysics 生物-生化与分子生物学
CiteScore
1.60
自引率
12.50%
发文量
68
审稿时长
6-12 weeks
期刊介绍: Doklady Biochemistry and Biophysics is a journal consisting of English translations of articles published in Russian in biochemistry and biophysics sections of the Russian-language journal Doklady Akademii Nauk. The journal''s goal is to publish the most significant new research in biochemistry and biophysics carried out in Russia today or in collaboration with Russian authors. The journal accepts only articles in the Russian language that are submitted or recommended by acting Russian or foreign members of the Russian Academy of Sciences. The journal does not accept direct submissions in English.
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