IL-23 Th17细胞在布鲁杆菌性脊柱炎中的作用研究

doi:10.3969/j.issn.1006-6233.2021.08.04

Abstract
Figure/Table
References
Related Citation (0)

Download: PDF (1247 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective: To investigate the roles of interleukin-23 (IL-23) and T helper cell 17 (Th17) in brucellosis spondylitis (BS). Methods: A total of 111 patients with BS admitted to the First Hospital Affiliated to Hebei North University from January 2015 to April 2020 were selected as the research objects, including 61 patients in acute phase (acute phase group) and 50 patients in chronic phase (chronic phase group), at the same time, 120 healthy controls were selected as the control group; the serum tube agglutination test (SAT) titer, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) were detected in patients with BS before treatment; the levels of serum L-23, IL-17, tumor necrosis factor-α (TNF-α), receptor activator of NF-κB ligand (RANKL) and matrix metalloproteinase-2 (MMP-2) were detected by enzyme linked immunosorbent assay (ELISA); Th17 cells level were detected by flow cytometry; Pearson method was used to analyze the correlation between serum IL-23 and Th17, between serum IL-23, Th17 and RANKL, MMP-2 in patients with BS. Results: The proportion of patients with SAT titer≥1∶100, CRP≥5mg/L and ESR≥20mm/h in acute phase group was higher than that in chronic phase group (P<0.05); compared with those in the control group, the Th17 cells, expression levels of serum TNF-α, IL-17, IL-23, RANKL and MMP-2 were higher in chronic phase group and acute phase group (P<0.05); compared with those in chronic phase group, the Th17 cells, expression levels of serum TNF-α, IL-17, IL-23, RANKL and MMP-2 in acute phase group were significantly higher (P<0.05); the level of IL-23 in BS patients was positively correlated with Th17 cells, RANKL and MMP-2 (P<0.05), and Th17 cells was positively correlated with RANKL and MMP-2 (P<0.05). Conclusion: IL-23 and Th17 may be involved in the pathogenesis of BS. This study may provide clinical basis for the study of BS.

Key words： Brucellosis spondylitis Interleukin-23 T helper cell 17

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors

Cite this article:

URL:

http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2021.08.04 OR http://www.hbyxzzs.cn/EN/Y2021/V27/I8/1251

[1] Liu X,Zheng M,Jiang Z,et al.Computed tomography imaging characteristics help to differentiate pyogenic spondylitis from brucellar spondylitis[J].Eur Spine,2020,29(7):1490~1498.
[2] Huang Q,Liao X,Yang S,et al.Brucellosis spondylitis[J].Int J Infect Dis,2020,95(1):462~463.
[3] 李社军.布鲁杆菌性脊柱炎的诊断及治疗[J].中国中西医结合外科杂志,2018,24(3):332~334.
[4] Kamali AN,Noorbakhsh SM,Hamedifar H,et al.A role for Th1-like Th17 cells in the pathogenesis of inflammatory and autoimmune disorders[J].Mol Immunol,2019,105(1):107~115.
[5] Mina R,Fariba K,Sanaz J,et al.Direct correlation between Th1 and Th17 responses in immunity to Brucella infection[J].Microbes Infect,2019,21(10):441~448.
[6] Villegas JA,Bayer AC,Ider K,et al.Il-23/Th17 cell pathway:A promising target to alleviate thymic inflammation maintenance in myasthenia gravis[J].Autoimmun,2019,98(1):59~73.
[7] 《中华传染病杂志》编辑委员会.布鲁菌病诊疗专家共识[J].中华传染病杂志,2017,35(12):705~710.
[8] 王守杰,王建莉,蔡志坚.Th17细胞及其在肿瘤免疫中作用的最新进展[J].中国肿瘤生物治疗杂志,2018,25(3):293~299.
[9] 韩丽红,舒凡,侯毅,等.急、慢性期布鲁菌病骨吸收相关细胞因子水平比较[J].中华地方病学杂志,2019,38(12):951~954.
[10] Giambartolomei GH,Arriola BPC,Victoria DM.Brucella and osteoarticular cell activation:partners in crime[J].Front Microbiol,2017,8(1):256~265.
[11] Kim AR,Kim JH,Choi YH,et al.The presence of neutrophils causes RANKL expression in periodontal tissue,giving rise to osteoclast formation[J].Periodontal Res,2020,55(6):868~876.
[12] Dizdar OS,Ozdemir AT,Baspinar O,et al.Serum prolidase level in patients with brucellosis and its possible relationship with pathogenesis of the disease:a prospective observational study[J].Turk Med Sci,2019,49(5):1479~1483.
[13] Funaki Y,Hasegawa Y,Okazaki R,et al.Resolvin E1 inhibits osteoclastogenesis and bone resorption by suppressing IL-17-induced RANKL expression in osteoblasts and RANKL-induced osteoclast differentiation[J].Yonago Acta Med,2018,61(1):8~18.
[14] Li W,Sun Y.Nrf2 is required for suppressing osteoclast RANKL-induced differentiation in RAW 264.7 cells via inactivating cannabinoid receptor type 2 with AM630[J].Regen Ther,2020,14(1):191~195.
[15] Razawy W,Van DM,Lubberts E.The role of IL-23 receptor signaling in inflammation-mediated erosive autoimmune arthritis and bone remodeling[J].Eur Immunol,2018,48(2):220~229.