人慢性根尖周炎及根尖囊肿组织巨噬细胞中IL-33的表达
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摘要
目的观察白细胞介素-33(interleukin-33,IL-33)在慢性根尖周炎及根尖囊肿组织巨噬细胞中的表达情况,为研究IL-33在根尖周病发病机制中的作用提供基础。方法收集正畸减数拔牙的无病变人牙根尖组织20例为正常对照组,慢性根尖周炎组织15例为慢性根尖周炎组,根尖囊肿组织15例为根尖囊肿组,分别进行HE染色,光学显微镜下观察根尖周组织的变化;以CD14作为巨噬细胞的标记,采用免疫荧光双染色法,在荧光显微镜下分别观察各组CD14阳性的巨噬细胞表达IL-33的情况。结果正常对照组、慢性根尖周炎组、根尖囊肿组中IL-33、CD14表达阳性的巨噬细胞密度分别为(23.81±5.16)个/mm~2、(62.97±8.54)个/mm~2、(119.83±14.61)个/mm~2;3组间差异具有统计学意义(F=87.17,P <0.01);根尖囊肿组IL-33、CD14表达阳性的巨噬细胞密度显著高于慢性根尖周炎组及对照组(P <0.01)。结论 IL-33、CD14表达阳性的巨噬细胞在正常根尖组织、慢性根尖周炎组织、根尖囊肿组织中依次增加。
Objective To observe the expression of interleukin-33(IL-33) in macrophages of chronic periapical periodontitis and apical cyst tissue, and to provide a basis for the study of the pathogenesis of IL-33 in periapical diseas-es. Methods The apical tissues of 20 normal control group, 15 chronic periapical periodontitis group and 15 apical cyst group were collected for HE staining and optical microscopy respectively. CD14 was used as the marker of macro-phages and double immunofluorescence staining was used to observe the changes of periapical tissues under fluores-cence microscopy. The expression of IL-33 in CD14-positive macrophages was observed. Results The macrophage density(cell/mm~2) of IL-33 and CD14 positive expression in normal control group, chronic periapical periodontitis group and root cyst group were(23.81 ± 5.16,62.97 ± 8.54,119.83 ± 14.61) respectively, and there were significant differenc-es among the three groups(F=87.17,P < 0.01). The density of IL-33 and CD14 positive macrophages in root cyst group was significantly higher than that in chronic periapical periodontitis group and control group(P < 0.01). Conclu-sion IL-33 and CD14 positive macrophages increased in normal apical tissue, chronic periapical periodontitis tissue and apical cyst tissue in turn.
Objective To observe the expression of interleukin-33(IL-33) in macrophages of chronic periapical periodontitis and apical cyst tissue, and to provide a basis for the study of the pathogenesis of IL-33 in periapical diseas-es. Methods The apical tissues of 20 normal control group, 15 chronic periapical periodontitis group and 15 apical cyst group were collected for HE staining and optical microscopy respectively. CD14 was used as the marker of macro-phages and double immunofluorescence staining was used to observe the changes of periapical tissues under fluores-cence microscopy. The expression of IL-33 in CD14-positive macrophages was observed. Results The macrophage density(cell/mm~2) of IL-33 and CD14 positive expression in normal control group, chronic periapical periodontitis group and root cyst group were(23.81 ± 5.16,62.97 ± 8.54,119.83 ± 14.61) respectively, and there were significant differenc-es among the three groups(F=87.17,P < 0.01). The density of IL-33 and CD14 positive macrophages in root cyst group was significantly higher than that in chronic periapical periodontitis group and control group(P < 0.01). Conclu-sion IL-33 and CD14 positive macrophages increased in normal apical tissue, chronic periapical periodontitis tissue and apical cyst tissue in turn.
引文
[1]Baba S,Kondo K,Kanaya K,et al.Expression of IL-33 and its receptor ST2 in chronic rhinosinusitis with nasal polyps[J].Laryngoscope,2014,124(4):e115-e122.
[2]Molofsky AB,Savage AK,Locksley RM.Interleukin-33 in tissue homeostasis,injury,and inflammation[J].Immunity,2015,42(6):1005-1019.
[3]Cayrol C,Girard JP.IL-33:an alarmin cytokine with crucial roles in innate immunity,inflammation and allergy[J].Curr Opin Immunol,2014,31:31-37.
[4]Velickovic M,Pejnovic N,Petrovic R,et al.Expression of interleukin-33 and its receptor ST2 in periapical granulomas and radicular cysts[J].J Oral Pathol Med,2016,45(1):70-76.
[5]Romano F,Graziano A,Spina A,et al.Increased early inflammatory response and osteoclastic activity in gingival tissues following conventional osseous resective surgery compared with the fibre retention technique:a pilot study[J].J Periodontal Res,2017,52(3):368-376.
[6]Li J,Wang R,Huang SG.Immunomodulatory activity of interleukin-27 in human chronic periapical diseases[J].Am J Transl Res,2017,9(3):1460-1470.
[7]Shen S,Wang R,Huang SG.Expression of the stem cell factor in fibroblasts,endothelialcells,and macrophages in periapical tissues in human chronic periapical diseases[J].Genet Mol Res,2017,16(1).Doi:10.4238/gmr16019394.
[8]Liang ZZ,Li J,Huang SG.Transforming growth factor beta-1 expression in macrophages of human chronic periapical diseases[J].Genet Mol Res,2017,16(1).Doi:10.4238/gmr16019329.
[9]Xu DM,Jiang HR,Kewin P,et al.IL-33 exacerbates antigen-induced arthritis by activating mast cells[J].Proc Natl Acad Sci U SA,2008,105(31):10913-10918.
[10]Joshi AD,Oak SR,Hartigan AJ,et al.Interleukin-33 contributes to both M1 and M2 chemokine marker expression in human macrophages[J].BMC Immunol,2010,11(10):52-55.
[11]Dougall WC.Molecular pathways:osteoclast-dependent and osteoclast-independent roles of the RANKL/RANK/OPG pathway in tumorigenesis and metastasis[J].Clin Cancer Res,2012,18(2):326-335.
[12]Liapatas S,Nakou M,Rontogianni D.Inflammatory infiltrate of chronic periradicular lesions:an immunohistochemical study[J].Int Endod J,2003,36(7):464-471.
[13]Bracks IV,Armada L,Goncalves LS.Distribution of mast cells and macrophages and expression of interleukin-6 in periapicalcysts[J].J Endod,2014,40(1):63-68.
[14]Schilling E,Weiss R,Grahnert A,et al.Molecular mechanism of LPS-induced TNF-alpha biosynthesis in polarized human macrophages[J].Mol Immunol,2018,93:206-215.
[2]Molofsky AB,Savage AK,Locksley RM.Interleukin-33 in tissue homeostasis,injury,and inflammation[J].Immunity,2015,42(6):1005-1019.
[3]Cayrol C,Girard JP.IL-33:an alarmin cytokine with crucial roles in innate immunity,inflammation and allergy[J].Curr Opin Immunol,2014,31:31-37.
[4]Velickovic M,Pejnovic N,Petrovic R,et al.Expression of interleukin-33 and its receptor ST2 in periapical granulomas and radicular cysts[J].J Oral Pathol Med,2016,45(1):70-76.
[5]Romano F,Graziano A,Spina A,et al.Increased early inflammatory response and osteoclastic activity in gingival tissues following conventional osseous resective surgery compared with the fibre retention technique:a pilot study[J].J Periodontal Res,2017,52(3):368-376.
[6]Li J,Wang R,Huang SG.Immunomodulatory activity of interleukin-27 in human chronic periapical diseases[J].Am J Transl Res,2017,9(3):1460-1470.
[7]Shen S,Wang R,Huang SG.Expression of the stem cell factor in fibroblasts,endothelialcells,and macrophages in periapical tissues in human chronic periapical diseases[J].Genet Mol Res,2017,16(1).Doi:10.4238/gmr16019394.
[8]Liang ZZ,Li J,Huang SG.Transforming growth factor beta-1 expression in macrophages of human chronic periapical diseases[J].Genet Mol Res,2017,16(1).Doi:10.4238/gmr16019329.
[9]Xu DM,Jiang HR,Kewin P,et al.IL-33 exacerbates antigen-induced arthritis by activating mast cells[J].Proc Natl Acad Sci U SA,2008,105(31):10913-10918.
[10]Joshi AD,Oak SR,Hartigan AJ,et al.Interleukin-33 contributes to both M1 and M2 chemokine marker expression in human macrophages[J].BMC Immunol,2010,11(10):52-55.
[11]Dougall WC.Molecular pathways:osteoclast-dependent and osteoclast-independent roles of the RANKL/RANK/OPG pathway in tumorigenesis and metastasis[J].Clin Cancer Res,2012,18(2):326-335.
[12]Liapatas S,Nakou M,Rontogianni D.Inflammatory infiltrate of chronic periradicular lesions:an immunohistochemical study[J].Int Endod J,2003,36(7):464-471.
[13]Bracks IV,Armada L,Goncalves LS.Distribution of mast cells and macrophages and expression of interleukin-6 in periapicalcysts[J].J Endod,2014,40(1):63-68.
[14]Schilling E,Weiss R,Grahnert A,et al.Molecular mechanism of LPS-induced TNF-alpha biosynthesis in polarized human macrophages[J].Mol Immunol,2018,93:206-215.