山东大学学报 (医学版) ›› 2021, Vol. 59 ›› Issue (6): 45-50.doi: 10.6040/j.issn.1671-7554.0.2021.0377
杜娇娇1,庄向华1,陈诗鸿1,王雪萌2,3,姜冬青1,吴菲1,韩晓琳2,华梦羽2,宋玉文1
DU Jiaojiao1, ZHUANG Xianghua1, CHEN Shihong1, WANG Xuemeng2,3, JIANG Dongqing1, WU Fei1, HAN Xiaolin2, HUA Mengyu2, SONG Yuwen1
摘要: 目的 分析白细胞介素-31(IL-31)和白细胞介素-33(IL-33)在绝经后骨质疏松症(PMOP)患者血清中的表达变化,探讨IL-31和IL-33与PMOP的关联性。 方法 选取绝经后女性共146例,使用双能 X 线骨密度仪(DXA)检测受试者的骨密度,根据骨密度将受试者分为三组:骨量正常组、低骨量组和骨质疏松组。测定血钙(Ca)、磷(P)、甲状旁腺激素(PTH)、25-羟基维生素D([25( OH)D])、IL-31、IL-33及骨转换指标血清骨特异性碱性磷酸酶(BALP)、血清1 型原胶原N-端前肽(P1NP)、血清抗酒石酸酸性磷酸酶(TRACP-5b)、血清1型胶原羧基端交联肽(β-CTX)的水平。比较不同骨量的绝经后女性血清IL-31、IL-33及骨转换指标的差异。 结果 三组受试者的血清IL-31浓度随着骨密度的降低而增加,而血清IL-33浓度随着骨密度的降低而下降,差异均有统计学意义(P<0.05)。多项式 Logistic回归分析结果显示,低骨量组中IL-33(OR:0.987,95%CI:0.974~0.999,P=0.030)差异有统计学意义,骨质疏松组中IL-31(OR:1.019,95%CI:1.009~1.028,P<0.001)、IL-33(OR:0.978,95%CI:0.960~0.995,P=0.013)差异有统计学意义,IL-33的OR值随着骨密度的降低呈下降趋势。提示IL-31和IL-33为PMOP的可能影响因素。 结论 IL-31为PMOP的可能危险因素,而IL-33为PMOP的可能保护因素,提示IL-31和IL-33在PMOP 发生过程中起重要作用。
中图分类号:
[1] Akkawi I, Zmerly H. Osteoporosis: current concepts [J]. Joints, 2018, 6(2): 122-127. [2] De Martinis M, Sirufo MM, Ginaldi L. Osteoporosis: current and emerging therapies targeted to immunological checkpoints [J]. Curr Med Chem, 2020, 27(37): 6356-6372. [3] Ponzetti M, Rucci N. Updates on osteoimmunology: whats new on the cross-talk between bone and immune system [J]. Front Endocrinol(Lausanne), 2019, 10: 236. doi: 10.3389/fendo.2019.00236. [4] Catalan-Dibene J, Mcintyre LL, Zlotnik A. Interleukin 30 to interleukin 40 [J]. J Interferon Cytokine Res, 2018, 38(10): 423-439. [5] Ginaldi L, De Martinis M, Ciccarelli F, et al. Increased levels of interleukin 31(IL-31)in osteoporosis [J]. BMC Immunol, 2015, 16: 60. doi: 10.1186/s12865-015-0125-9. [6] Ginaldi L, De Martinis M, Saitta S, et al. Interleukin-33 serum levels in postmenopausal women with osteoporosis [J]. Sci Rep, 2019, 9(1): 3786. [7] Petra AI, Tsilioni I, Taracanova A, et al. Interleukin 33 and interleukin 4 regulate interleukin 31 gene expression and secretion from human laboratory of allergic diseases 2 mast cells stimulated by substance P and/or immunoglobulin E [J]. Allergy Asthma Proc, 2018, 39(2): 153-160. [8] Cheung PF, Wong CK, Ho AW, et al. Activation of human eosinophils and epidermal keratinocytes by Th2 cytokine IL-31: implication for the immunopathogenesis of atopic dermatitis [J]. Int Immunol, 2010, 22(6): 453-467. [9] Dillon SR, Sprecher C, Hammond A, et al. Interleukin 31, a cytokine produced by activated T cells, induces dermatitis in mice [J]. Nat Immunol, 2004, 5(7): 752-760. [10] Dambacher J, Beigel F, Seiderer J, et al. Interleukin 31 mediates MAP kinase and STAT1/3 activation in intestinal epithelial cells and its expression is upregulated in inflammatory bowel disease [J]. Gut, 2007, 56(9): 1257-1265. [11] Lee CH, Hong CH, Yu WT, et al. Mechanistic correlations between two itch biomarkers, cytokine interleukin-31 and neuropeptide beta-endorphin, via STAT3/calcium axis in atopic dermatitis [J]. Br J Dermatol, 2012, 167(4): 794-803. [12] Chattopadhyay S, Tracy E, Liang P, et al. Interleukin-31 and oncostatin-M mediate distinct signaling reactions and response patterns in lung epithelial cells [J]. J Biol Chem, 2007, 282(5): 3014-3026. [13] Takayanagi H. Osteoimmunology in 2014: Two-faced immunology-from osteogenesis to bone resorption [J]. Nat Rev Rheumatol, 2015, 11(2): 74-76. [14] 夏维波,章振林,林华,等. 原发性骨质疏松症诊疗指南(2017)[J]. 中华骨质疏松和骨矿盐疾病杂志, 2019, 25(3): 281-309. [15] Azizieh FY, Shehab D, Al JK, et al. Circulatory pattern of cytokines, adipokines and bone markers in postmenopausal women with low BMD [J]. J Inflamm Res, 2019, 12: 99-108. doi: 10.2147/JIR.S203590. [16] Cop N, Ebo DG, Bridts CH, et al. Influence of IL-6, IL-33, and TNF-alpha on human mast cell activation: Lessons from single cell analysis by flow cytometry [J]. Cytometry B Clin Cytom, 2018, 94(3): 405-411. [17] Stott B, Lavender P, Lehmann S, et al. Human IL-31 is induced by IL-4 and promotes TH2-driven inflammation [J]. J Allergy Clin Immunol, 2013, 132(2): 446-454. [18] Schnittker D, Kwofie K, Ashkar A, et al. Oncostatin M and TLR-4 ligand synergize to induce MCP-1, IL-6, and VEGF in human aortic adventitial fibroblasts and smooth muscle cells [J]. Mediators Inflamm, 2013, 2013: 317503. doi: 10.1155/2013/317503. [19] Rosine N, Etcheto A, Hendel-Chavez H, et al. Increase in Il-31 serum levels is associated with reduced structural damage in early axial spondyloarthritis [J]. Sci Rep, 2018, 8(1): 7731. [20] Cornelissen C, Luscher-Firzlaff J, Baron JM, et al. Signaling by IL-31 and functional consequences [J]. Eur J Cell Biol, 2012, 91(6-7): 552-566. [21] Zhang Q, Putheti P, Zhou Q, et al. Structures and biological functions of IL-31 and IL-31 receptors [J]. Cytokine Growth Factor Rev, 2008, 19(5-6): 347-356. [22] Perrigoue JG, Li J, Zaph C, et al. IL-31-IL-31R interactions negatively regulate type 2 inflammation in the lung [J]. J Exp Med, 2007, 204(3): 481-487. [23] De Martinis M, Franceschi C, Monti D, et al. Inflamm-ageing and lifelong antigenic load as major determinants of ageing rate and longevity [J]. FEBS Lett, 2005, 579(10): 2035-2039. [24] Zhao R. Immune regulation of osteoclast function in postmenopausal osteoporosis: a critical interdisciplinary perspective [J]. Int J Med Sci, 2012, 9(9): 825-832. [25] Inada M, Miyaura C. Cytokines in bone diseases. Cytokine and postmenopausal osteoporosis [J]. Clin Calcium, 2010, 20(10): 1467-1472. [26] Ginaldi L, De Martinis M. Osteoimmunology and Beyond [J]. Curr Med Chem, 2016, 23(33): 3754-3774. [27] Zoltowska NA, Lei Y, Adner M, et al. Mast cell-dependent IL-33/ST2 signaling is protective against the development of airway hyperresponsiveness in a house dust mite mouse model of asthma [J]. Am J Physiol Lung Cell Mol Physiol, 2018, 314(3): 484-492. [28] Saidi S, Bouri F, Lencel P, et al. IL-33 is expressed in human osteoblasts, but has no direct effect on bone remodeling [J]. Cytokine, 2011, 53(3): 347-354. [29] Schulze J, Bickert T, Beil FT, et al. Interleukin-33 is expressed in differentiated osteoblasts and blocks osteoclast formation from bone marrow precursor cells [J]. J Bone Miner Res, 2011, 26(4): 704-717. [30] Velickovic M, Pejnovic N, Mitrovic S, et al. ST2 deletion increases inflammatory bone destruction in experimentally induced periapical lesions in mice [J]. J Endod, 2015, 41(3): 369-375. [31] Zaiss MM, Kurowska-Stolarska M, Bohm C, et al. IL-33 shifts the balance from osteoclast to alternatively activated macrophage differentiation and protects from TNF-alpha-mediated bone loss [J]. J Immunol, 2011, 186(11): 6097-6105. [32] Taichman RS, Reilly MJ, Matthews LS. Human osteoblast-like cells and osteosarcoma cell lines synthesize macrophage inhibitory protein 1alpha in response to interleukin 1beta and tumour necrosis factor alpha stimulation in vitro [J]. Br J Haematol, 2000, 108(2): 275-283. [33] Da LF, Oliveira AP, Borges D, et al. The physiopathological role of IL-33: new highlights in bone biology and a proposed role in periodontal disease [J]. Mediators Inflamm, 2014, 2014: 342410. doi: 10.1155/2014/342410. [34] Saleh H, Eeles D, Hodge JM, et al. Interleukin-33, a target of parathyroid hormone and oncostatin m, increases osteoblastic matrix mineral deposition and inhibits osteoclast formation in vitro [J]. Endocrinology, 2011, 152(5): 1911-1922. [35] Saluja R, Ketelaar ME, Hawro T, et al. The role of the IL-33/IL-1RL1 axis in mast cell and basophil activation in allergic disorders [J]. Mol Immunol, 2015, 63(1): 80-85. [36] Di Salvo E, Ventura-Spagnolo E, Casciaro M, et al. IL-33/IL-31 axis: a potential inflammatory pathway [J]. Mediators Inflamm, 2018, 2018: 3858032. doi: 10.1155/2018/3858032. [37] Brylka LJ, Schinke T. Chemokines in physiological and pathological bone remodeling [J]. Front Immunol, 2019, 10: 2182. doi: 10.3389/fimmu.2019.02182. |
[1] | 康成为,刘雷,蒲小兵,谭钢,董长超,晏兆魁. 合并亚临床型甲状腺功能减退的骨质疏松症62例患者骨代谢及骨转换标志物水平分析[J]. 山东大学学报 (医学版), 2020, 58(5): 82-86. |
[2] | 蔡秋景,张倩,何学佳,孙文丽,郭爱丽,张楠,朱薇薇. 气道平滑肌细胞通过TGF-β1/Smad3信号通路调节IL-33的表达参与哮喘[J]. 山东大学学报 (医学版), 2020, 58(4): 78-83. |
[3] | 李娜,张志勉. 138例39~81岁体检人员血管钙化指标的关联分析[J]. 山东大学学报 (医学版), 2020, 58(2): 85-89. |
[4] | 徐大霞,侯楠,李晓峰,王闯,孔猛,焦广俊,陈允震. 糖皮质激素性骨质疏松症骨代谢与糖皮质激素用药时间的相关性[J]. 山东大学学报(医学版), 2017, 55(5): 103-107. |
[5] | 张婧,郝兰香,张晓晨,张永红,范珊珊,刘燕,蒋玲. 双酚A对大鼠椎体及股骨骨密度的影响[J]. 山东大学学报(医学版), 2016, 54(3): 36-40. |
[6] | 冯潇雨, 张洪美, 车选强, 康东红. 成骨细胞刺激因子对去卵巢骨质疏松大鼠的治疗效果[J]. 山东大学学报(医学版), 2015, 53(7): 8-12. |
[7] | 张丽, 严红. 2型糖尿病患者骨质疏松情况调查[J]. 山东大学学报(医学版), 2014, 52(S2): 107-107. |
[8] | 张洪美1,王燕2,康东红1,曹维1,刘涛1,王萍1. 济南市城区健康成年男性腰椎和股骨的骨密度分析[J]. 山东大学学报(医学版), 2013, 51(4): 67-70. |
[9] | 成开花1,张立新2. 促性腺激素释放激素激动剂治疗子宫内膜异位症对性激素及骨密度的影响及处理方法[J]. 山东大学学报(医学版), 2012, 50(3): 83-86. |
[10] | 刘梅1,张君2,王旭霞3. T1DM、T2DM糖尿病大鼠牙槽骨骨密度变化的相关性实验研究[J]. 山东大学学报(医学版), 2011, 49(9): 53-. |
[11] | 张磊,李牧,祁磊,蔡中续,李玉华,孙元亮. 晚期糖基化终末产物在糖尿病大鼠骨质疏松发病中的作用及胰岛素潜在的防护机制[J]. 山东大学学报(医学版), 2007, 45(11): 1148-1152. |
[12] | 孙秀江,王韶进,刘文广,王兴山 . 全膝关节置换术后假体周围骨密度的临床观察[J]. 山东大学学报(医学版), 2006, 44(12): 1265-1267. |
Viewed | ||||||||||||||||||||||||||||||||||||||||||||||||||
Full text 145
|
|
|||||||||||||||||||||||||||||||||||||||||||||||||
Abstract 1777
|
|
|||||||||||||||||||||||||||||||||||||||||||||||||
Cited |
|
|||||||||||||||||||||||||||||||||||||||||||||||||
Shared | ||||||||||||||||||||||||||||||||||||||||||||||||||
Discussed |
|