非创伤性股骨头坏死患者血清白细胞介素-33水平变化及意义
|
摘要
目的探讨非创伤性股骨头坏死(NONFH)患者血清白细胞介素-33(IL-33)水平变化及意义。方法选取2017年7月至2018年6月徐州医科大学附属邳州市人民医院门诊或病房诊治的NONFH患者50例为观察组(NONFH组),另选择同期体检中心接受体检的健康成年人50例为对照组。所有人员清晨空腹时采集肘静脉血2 ml,分离血清,采用双抗体夹心酶联免疫吸附实验(ELISA)检测两组人群血清中IL-33水平并比较。同时分析NONFH组中不同致病原因、不同国际骨循环研究协会(ARCO)分期、有无塌陷对患者血清IL-33水平的影响。结果 NONFH组患者血清中IL-33水平均明显高于健康人群血清水平[(11.1±4.5)pg/ml vs(6.3±2.4)pg/ml,t=6.655,P=0.000]。激素性NONFH、酒精性NONFH、原发性NONFH患者血清IL-33水平比较无统计学差异[(10.3±8.3)pg/ml、(12.5±8.8)pg/ml、(11.7±5.9)pg/ml,F=0.478,P=0.623]。ARCOⅡ、Ⅲ、Ⅳ期患者血清IL-33水平比较无统计学差异[(11.9±8.4)pg/ml、(13.6±6.3)pg/ml、(12.1±7.5)pg/ml,F=0.278,P=0.759]。股骨头有、无塌陷患者血清IL-33水平比较无统计学差异[(11.7±6.9)pg/ml vs(9.9±4.1)pg/ml,t=1.159,P=0.235]。结论 NONFH患者的血清IL-33水平明显高于健康人群水平,提示IL-33可能作为一种促炎细胞因子参与NONFH病情活动,且与发病原因、有无股骨头塌陷、NONFH分期无关。
Objective To investigate the changes and significance of serum interleukin-33(IL-33) level in patients with non-traumatic femoral head necrosis(NONFH).Methods Fifty patients with NONFH who received treatment in Pizhou People′s Hospital from July 2017 to June 2018 were selected as observation group(NONFH group)and 50 healthy adults who received physical examination at the same period were selected as control group.The elbow venous blood was collected at fasting in the morning,and the serum was separated.The serum level of IL-33 was detected by double antibody sandwich enzyme-linked immunosorbent assay(ELISA).The serum levels of IL-33 were compared between two groups,and the effects of different pathogenic factors,ARCO stages and femoral head collapse on serum IL-33 level in NONFH group were analyzed.Results The serum level of IL-33 in NONFH group was significantly higher than that in healthy people [(11.1±4.5)pg/ml vs(6.3±2.4)pg/ml,t=6.655,P=0.000].There was no significant difference in serum IL-33 levels among steroid-induced avascular necrosis,alcoholic avascular necrosis and primary avascular necrosis of femoral head[(10.3±8.3)pg/ml,(12.5±8.8)pg/ml,(11.7±5.9)pg/ml,F=0.478,P=0.623].There was no significant difference in serum IL-33 levels among ARCO stage Ⅱ,Ⅲ and Ⅳ patients[(11.9±8.4)pg/ml,(13.6±6.3)pg/ml,(12.1±7.5)pg/ml,F=0.278,P=0.759].There was no significant difference in serum IL-33 levels between patients with and without femoral head collapse[(11.7±6.9)pg/ml vs(9.9±4.1)pg/ml,t=1.159,P=0.235].Conclusion The serum level of IL-33 in patients with NONFH was significantly higher than that in healthy people,suggesting that IL-33 may be involved in the activity of NONFH as a proinflammatory cytokine,and not related to the etiology,femoral head collapse and NONFH stage.
Objective To investigate the changes and significance of serum interleukin-33(IL-33) level in patients with non-traumatic femoral head necrosis(NONFH).Methods Fifty patients with NONFH who received treatment in Pizhou People′s Hospital from July 2017 to June 2018 were selected as observation group(NONFH group)and 50 healthy adults who received physical examination at the same period were selected as control group.The elbow venous blood was collected at fasting in the morning,and the serum was separated.The serum level of IL-33 was detected by double antibody sandwich enzyme-linked immunosorbent assay(ELISA).The serum levels of IL-33 were compared between two groups,and the effects of different pathogenic factors,ARCO stages and femoral head collapse on serum IL-33 level in NONFH group were analyzed.Results The serum level of IL-33 in NONFH group was significantly higher than that in healthy people [(11.1±4.5)pg/ml vs(6.3±2.4)pg/ml,t=6.655,P=0.000].There was no significant difference in serum IL-33 levels among steroid-induced avascular necrosis,alcoholic avascular necrosis and primary avascular necrosis of femoral head[(10.3±8.3)pg/ml,(12.5±8.8)pg/ml,(11.7±5.9)pg/ml,F=0.478,P=0.623].There was no significant difference in serum IL-33 levels among ARCO stage Ⅱ,Ⅲ and Ⅳ patients[(11.9±8.4)pg/ml,(13.6±6.3)pg/ml,(12.1±7.5)pg/ml,F=0.278,P=0.759].There was no significant difference in serum IL-33 levels between patients with and without femoral head collapse[(11.7±6.9)pg/ml vs(9.9±4.1)pg/ml,t=1.159,P=0.235].Conclusion The serum level of IL-33 in patients with NONFH was significantly higher than that in healthy people,suggesting that IL-33 may be involved in the activity of NONFH as a proinflammatory cytokine,and not related to the etiology,femoral head collapse and NONFH stage.
引文
[1] Baekkevold ES,Roussigné M,Ymnanaka T,et al.Molecular characterization of NF-HEV,a nuclear factor preferentially expressed in human high endothelial venules[J].Am J Path,2003,163(1):69-79.
[2] Schmitz J,Owyang A,Oldham E,et al.IL-33,an interleukin-1 like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines[J].Immunity,2005,23(5):479-490.
[3] Carriere V,Roussel L,Ortega N,et al.IL-33,the IL-1-like cytokine ligand for ST2 receptor,is a chromatin-associated nuclear factor in vivo[J].Proc Natl Acad Sci USA,2007,104(1):282-287.
[4] Frommer KW,Neumann E,Lange U.Inflammation and bone:osteoimmunological aspects[J].Z Rheumatol,2016,75(5):444-450.
[5] 李子荣.股骨头坏死临床诊疗规范[J].中华骨与关节外科杂志.2015,9 (1):1-6.
[6] Sugano N,Atsumi T,Ohzono K,et al.The 2001 revised criteria for diagnosis,classification,and staging of idiopathic osteonecrosis of the femoral head[J].J Orthop Sci,2002,7(5):601-605.
[7] Mankin HJ.Nontraumatic necrosis of bone (osteonecrosis) [J].N Engl J Med,1992,326(22):1473-1479.
[8] Leung BP,Xu D,Culshaw S,et al.A novel therapy of murine collagen-induced arthritis with soluble T1/SrI2[J].Immunology,2004,173(1):145-150.
[9] Mu R,Huang HQ,Li YH,et al.Elevated serum interleukin-33 is associated with autoantibody production in patients with rheumatoid arthritis[J].J Rheumatol,2010,37 (10):2006-2013.
[10] Omata,Y,Frech M,Primbs T,et al.Group 2 innate lymphoid cells attenuate inflammatory arthritis and protect from bone destruction in mice[J].Cell Rep,2018,24(1):169-180.
[11] Dalmas E,Lehmann FM,Dror E,et al.Interleukin-33-activated islet-resident innate lymphoid cells promote insulin secretion through myeloid cell retinoic acid production[J].Immunity,2017,47(5):928-942,e7.
[12] Wang Y,Chen Z,Huang Y,et al.Prognostic significance of serum interleukins and soluble ST2 in Traditional Chinese Medicine (TCM) syndrome-differentiated rheumatoid arthritis[J].Med SciMonit,2018,24:3472-3478.
[2] Schmitz J,Owyang A,Oldham E,et al.IL-33,an interleukin-1 like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines[J].Immunity,2005,23(5):479-490.
[3] Carriere V,Roussel L,Ortega N,et al.IL-33,the IL-1-like cytokine ligand for ST2 receptor,is a chromatin-associated nuclear factor in vivo[J].Proc Natl Acad Sci USA,2007,104(1):282-287.
[4] Frommer KW,Neumann E,Lange U.Inflammation and bone:osteoimmunological aspects[J].Z Rheumatol,2016,75(5):444-450.
[5] 李子荣.股骨头坏死临床诊疗规范[J].中华骨与关节外科杂志.2015,9 (1):1-6.
[6] Sugano N,Atsumi T,Ohzono K,et al.The 2001 revised criteria for diagnosis,classification,and staging of idiopathic osteonecrosis of the femoral head[J].J Orthop Sci,2002,7(5):601-605.
[7] Mankin HJ.Nontraumatic necrosis of bone (osteonecrosis) [J].N Engl J Med,1992,326(22):1473-1479.
[8] Leung BP,Xu D,Culshaw S,et al.A novel therapy of murine collagen-induced arthritis with soluble T1/SrI2[J].Immunology,2004,173(1):145-150.
[9] Mu R,Huang HQ,Li YH,et al.Elevated serum interleukin-33 is associated with autoantibody production in patients with rheumatoid arthritis[J].J Rheumatol,2010,37 (10):2006-2013.
[10] Omata,Y,Frech M,Primbs T,et al.Group 2 innate lymphoid cells attenuate inflammatory arthritis and protect from bone destruction in mice[J].Cell Rep,2018,24(1):169-180.
[11] Dalmas E,Lehmann FM,Dror E,et al.Interleukin-33-activated islet-resident innate lymphoid cells promote insulin secretion through myeloid cell retinoic acid production[J].Immunity,2017,47(5):928-942,e7.
[12] Wang Y,Chen Z,Huang Y,et al.Prognostic significance of serum interleukins and soluble ST2 in Traditional Chinese Medicine (TCM) syndrome-differentiated rheumatoid arthritis[J].Med SciMonit,2018,24:3472-3478.