细胞因子、粘附分子和毒性蛋白在鼻息肉中的表达及意义
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摘要
目的：探讨鼻息肉组织中嗜酸性粒细胞阳离子蛋白（ECP）、粘附分子E-选择素（E-selectin）和前炎症细胞因子粒细胞-巨噬细胞集落刺激因子（GM-CSF）水平及其在鼻息肉病理机理中的相关性。
方法：采用酶联免疫吸附测定（enzyme linked immunosoent assay，ELISA）检测60例鼻息肉组织匀浆中ECP、E-selectin和GM-CSF水平，以12例鼻中隔手术患者之代偿肥大的下鼻甲后端粘膜作为对照。
结果：鼻息肉组ECP浓度为293.72±56.87μg/L，对照组69.17±14.75μg/L；鼻息肉组E-selectin浓度为42.58±13.52μg/L，对照组为11.35±3.17μg/L；鼻息肉组GM-CSF浓度为83.75±38.58ng/L，对照组为9.87±2.22ng/L。鼻息肉组织匀浆中ECP、E-selectin和GM-CSF水平均明显高于对照组，差异极显著（P﹤0.001）。三种分子在鼻息肉中的表达相互间呈显著正相关。
结论：ECP、E-selectin和GM-CSF相互协同作用，通过参与嗜酸性粒细胞等炎症细胞的浸润，活化，增殖，从而在鼻息肉的形成过程中起重要作用。
Objective: To study significance of Eosinophil cationic protein (ECP), E-selectin and granulocyte-macrophage colony stimulation factor (GM-CSF) in nasal polyps.
Methods: The ECP, E-selectin and GM-CSF were measured by enzyme linked immunosorbent assay (ELISA) in group of 60 cases and 12 control cases from normal inferior turbinates respectively.
Results: The level of ECP in nasal polyps group was 293.72±56.87μg/L, while in control groups was 69.17±14.75μg/L; The level of E-selectin was 42.58±13.52μg/L，in control group was 11.35±3.17μg/L, The level of GM-CSF was 83.75±38.58ng/L, in control
group was 9.87±2.22ng/L. The level of ECP, GM-CSF and E-selectin in nasal polyps groups was significantly higer than those of controls(P<0.001). And the strong positive correlations were observed among the three participants.
Conclusion: This study demonstrate that the secretion of ECP, E-selectin and GM-CSF increase significantly in nasal polyps. They may involve the occurrence of nasal polyps by activiting on eosinophils.
方法：采用酶联免疫吸附测定（enzyme linked immunosoent assay，ELISA）检测60例鼻息肉组织匀浆中ECP、E-selectin和GM-CSF水平，以12例鼻中隔手术患者之代偿肥大的下鼻甲后端粘膜作为对照。
结果：鼻息肉组ECP浓度为293.72±56.87μg/L，对照组69.17±14.75μg/L；鼻息肉组E-selectin浓度为42.58±13.52μg/L，对照组为11.35±3.17μg/L；鼻息肉组GM-CSF浓度为83.75±38.58ng/L，对照组为9.87±2.22ng/L。鼻息肉组织匀浆中ECP、E-selectin和GM-CSF水平均明显高于对照组，差异极显著（P﹤0.001）。三种分子在鼻息肉中的表达相互间呈显著正相关。
结论：ECP、E-selectin和GM-CSF相互协同作用，通过参与嗜酸性粒细胞等炎症细胞的浸润，活化，增殖，从而在鼻息肉的形成过程中起重要作用。
Objective: To study significance of Eosinophil cationic protein (ECP), E-selectin and granulocyte-macrophage colony stimulation factor (GM-CSF) in nasal polyps.
Methods: The ECP, E-selectin and GM-CSF were measured by enzyme linked immunosorbent assay (ELISA) in group of 60 cases and 12 control cases from normal inferior turbinates respectively.
Results: The level of ECP in nasal polyps group was 293.72±56.87μg/L, while in control groups was 69.17±14.75μg/L; The level of E-selectin was 42.58±13.52μg/L，in control group was 11.35±3.17μg/L, The level of GM-CSF was 83.75±38.58ng/L, in control
group was 9.87±2.22ng/L. The level of ECP, GM-CSF and E-selectin in nasal polyps groups was significantly higer than those of controls(P<0.001). And the strong positive correlations were observed among the three participants.
Conclusion: This study demonstrate that the secretion of ECP, E-selectin and GM-CSF increase significantly in nasal polyps. They may involve the occurrence of nasal polyps by activiting on eosinophils.
引文
Jankowski R. Eosinophils in the pathophysiology of nasal polyposis [J]. Acta Otolaryngol, 1996, 116(2):160-163.
Allen JS, Eisma K, Leonard G, et al. Interleukin-3, Interleukin-5, Granulocyte Macrophage-colony stimulating factor expression in nasal polyps [J]. Am J Otolaryngol, 1997, 18(3):239-246.
董震，关桂梅，常万龙。鼻息肉组织中细胞增殖与凋亡相关基因蛋白的表达及意义[J]。中华耳鼻咽喉科杂志，2000，35（6）：429-431。
Venge P, Bystr?m J, Carlson M, et al. ECP:molecular and biological properties and the use of ECP as a marker of eosinophil activation in disease [J]. Clin Exp Allergy, 1999; 29(9):1172-1186.
Papon JF, Coste A, Gendron MC, et al. HLA-DR and ICAM-1 expression and modulation in epithelial cells from nasal polyps [J]. Laryngoscope, 2002, 112(12): 2067-2075.
Simon SL, Hu Y, Vestweber D, et al. Neutrophil tethering on E-selectin activates beta 2-intergrin binding to ICAM-1 through a mitogen-activated protein kinase signal transduction pathway [J]. J Immunol, 2000, 164(12): 4348-4358.
Goda K, Tanaka T, Monden M, et al. Characterization of an apparently conserved epitope in E- and P-selectin identified by dual-specific monoclonal antibodies [J]. Eur Immunol, 1999, 29(8): 1551-1560.
Lisa B, Cristiana S, Dawson B. et al. Allergens, IgE, medators inflammatory mechanisms [J]. J Allergy Clin Immunol. 199814(7):766-780.
Venge P, Byst?m J. Molecules in focus Eosinophil catonic protein(ECP) [J]. Intel J Biochemistry & Cell bio;1998(4);30:433-437.
Cosset P, Tillie-leblond I, Janin A, et al. Expression of E-selectin, ICAM-1 and VCAM-1 on bronchial biopsies from allergic and non-allergic asthmatic patients [J].
Int Arch Allergy Immunol, 199;106(1): 69-77.
Coste A, Brugel L, Maitre B, et al. Inflammatory cells as well as epithelial cells in nasal polyps express vascular endothelial growth factor [J]. Eur Respir J, 200, 15(2): 367-372.
Bousquet J, Van Cauwenberge P, Khaltaev N,et al. Allergic rhinitis and its impact on asthma[J]. J Allergy Clin Immunol, 2001 Nov; 108(5 Suppl): S147-334.
Rudack C, Hauser U, Stoll W. Effect of cytokines and fibroblasts on eosinophilic granulocyte survival in polyposis nasi [J]. Laryngorhinootologie, 1999; 78(7): 378-381.
Erjefalt JS, greiff L, Andersson M, et al. Degranulation paterns of eosinophil granulocytes as determinants of eosinophil driven disease [J]. Thorax. 2001 Feb; 56:341-344.
Watanabe K, Misu T, Inoue S, et al. Cytolysis of eosinophils in nasal secretions [J]. Ann Otol Rhinol Laryngol. 2003 Feb; 112(2): 169-173.
Roca Ferrer J, Mullol J, Xaubet A, et al. Proinflamatory cytokines and eosinophil cationic protein on glandular secretion from human nasal mucosa: regulaion by corticoseroids [J]. J Allergy Clin Immunol. 2001 Jul; 108(1):87-93.
Simon HU, Weber M, Becker E, et al. Eosinophils maintain their capacity to signal and release eosinophil cationic protein upon repetitive stimulation with the same agonist [J]. J Immunol. 2000 Oct; 165(7):4069-4075.
Allen JS, Eisma K, Leonard G, et al. Interleukin-3, Interleukin-5, Granulocyte Macrophage-colony stimulating factor expression in nasal polyps [J]. Am J Otolaryngol, 1997, 18(3):239-246.
董震，关桂梅，常万龙。鼻息肉组织中细胞增殖与凋亡相关基因蛋白的表达及意义[J]。中华耳鼻咽喉科杂志，2000，35（6）：429-431。
Venge P, Bystr?m J, Carlson M, et al. ECP:molecular and biological properties and the use of ECP as a marker of eosinophil activation in disease [J]. Clin Exp Allergy, 1999; 29(9):1172-1186.
Papon JF, Coste A, Gendron MC, et al. HLA-DR and ICAM-1 expression and modulation in epithelial cells from nasal polyps [J]. Laryngoscope, 2002, 112(12): 2067-2075.
Simon SL, Hu Y, Vestweber D, et al. Neutrophil tethering on E-selectin activates beta 2-intergrin binding to ICAM-1 through a mitogen-activated protein kinase signal transduction pathway [J]. J Immunol, 2000, 164(12): 4348-4358.
Goda K, Tanaka T, Monden M, et al. Characterization of an apparently conserved epitope in E- and P-selectin identified by dual-specific monoclonal antibodies [J]. Eur Immunol, 1999, 29(8): 1551-1560.
Lisa B, Cristiana S, Dawson B. et al. Allergens, IgE, medators inflammatory mechanisms [J]. J Allergy Clin Immunol. 199814(7):766-780.
Venge P, Byst?m J. Molecules in focus Eosinophil catonic protein(ECP) [J]. Intel J Biochemistry & Cell bio;1998(4);30:433-437.
Cosset P, Tillie-leblond I, Janin A, et al. Expression of E-selectin, ICAM-1 and VCAM-1 on bronchial biopsies from allergic and non-allergic asthmatic patients [J].
Int Arch Allergy Immunol, 199;106(1): 69-77.
Coste A, Brugel L, Maitre B, et al. Inflammatory cells as well as epithelial cells in nasal polyps express vascular endothelial growth factor [J]. Eur Respir J, 200, 15(2): 367-372.
Bousquet J, Van Cauwenberge P, Khaltaev N,et al. Allergic rhinitis and its impact on asthma[J]. J Allergy Clin Immunol, 2001 Nov; 108(5 Suppl): S147-334.
Rudack C, Hauser U, Stoll W. Effect of cytokines and fibroblasts on eosinophilic granulocyte survival in polyposis nasi [J]. Laryngorhinootologie, 1999; 78(7): 378-381.
Erjefalt JS, greiff L, Andersson M, et al. Degranulation paterns of eosinophil granulocytes as determinants of eosinophil driven disease [J]. Thorax. 2001 Feb; 56:341-344.
Watanabe K, Misu T, Inoue S, et al. Cytolysis of eosinophils in nasal secretions [J]. Ann Otol Rhinol Laryngol. 2003 Feb; 112(2): 169-173.
Roca Ferrer J, Mullol J, Xaubet A, et al. Proinflamatory cytokines and eosinophil cationic protein on glandular secretion from human nasal mucosa: regulaion by corticoseroids [J]. J Allergy Clin Immunol. 2001 Jul; 108(1):87-93.
Simon HU, Weber M, Becker E, et al. Eosinophils maintain their capacity to signal and release eosinophil cationic protein upon repetitive stimulation with the same agonist [J]. J Immunol. 2000 Oct; 165(7):4069-4075.