您的位置:山东大学 -> 科技期刊社 -> 《山东大学学报(医学版)》

山东大学学报(医学版) ›› 2014, Vol. 52 ›› Issue (10): 25-28.doi: 10.6040/j.issn.1671-7554.0.2014.144

• 基础医学 • 上一篇    下一篇

阿奇霉素和地塞米松对烟曲霉孢子刺激A549细胞分泌ICAM-1和TNF-α的影响

吴凤娟1, 李陶2, 亓倩3, 李玉2   

  1. 1. 菏泽市立医院呼吸科, 山东 菏泽 274007;
    2. 山东大学齐鲁医院呼吸科, 山东 济南 250012;
    3. 山东大学医学院, 山东 济南 250012
  • 收稿日期:2014-03-17 修回日期:2014-06-10 出版日期:2014-10-10 发布日期:2014-10-10
  • 通讯作者: 李玉。E-mail:qlliyu@163.com E-mail:qlliyu@163.com

Effects of azithromycin and dexamethasone on the secretion of ICAM-1 and TNF-α in A549 cells stimulated with Aspergillus fumigatus conidia

WU Fengjuan1, LI Tao2, QI Qian3, LI Yu2   

  1. 1. Department of Pulmonary Disease, Heze Municipal Hospital, Heze 274007, Shandong, China;
    2. Department of Pulmonary Disease, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China;
    3. School of Medicine, Shandong University, Jinan 250012, Shandong, China
  • Received:2014-03-17 Revised:2014-06-10 Online:2014-10-10 Published:2014-10-10

摘要: 目的 观察阿奇霉素和地塞米松对烟曲霉孢子刺激A549细胞分泌ICAM-1和TNF-α的影响。方法 以正常培养的A549细胞为对照,采用ELISA方法检测A549细胞与烟曲霉孢子共孵育4、24 h后细胞分泌ICAM-1和TNF-α的水平,并在细胞与孢子共孵育24 h基础上,分别加入阿奇霉素(0.5、2.5 mg/L)和地塞米松(0.5、2.5 mg/L),比较不同药物浓度对两种细胞因子水平的影响。结果 A549细胞与烟曲霉孢子共孵4、24 h后,细胞释放ICAM-1和TNF-α的浓度均较对照组明显升高(P<0.05);与单纯烟曲霉孢子刺激相比,2.5 mg/L阿奇霉素明显抑制与烟曲霉孢子共孵的细胞分泌TNF-α(P<0.05),2.5 mg/L地塞米松明显抑制与烟曲霉孢子共孵的细胞分泌ICAM-1和TNF-α(P<0.05)。结论 阿奇霉素和地塞米松均可以抑制烟曲霉孢子诱导的炎性因子释放,减轻炎症反应及肺损伤。

关键词: A549细胞, 细胞因子, 地塞米松, 烟曲霉孢子, 阿奇霉素

Abstract: Objective To evaluate the effect of azithromycin and dexamethasone on the secretion of ICAM-1 and TNF-α in A549 cells stimulated with Aspergillus fumigatus conidia. Methods The concentrations of ICAM-1 and TNF-α were detected by ELISA when A549 cells were cultured alone and were cultured with Aspergillus fumigatus conidia for 4 and 24 hours. The normal cultured A549 cells were taken as control group. After being cultured with conidia for 24 hours, A549 cells were treatd with azithromycin (0.5, 2.5 mg/L) or dexamethasone (0.5, 2.5 mg/L) and then the ICAM-1 and TNF-α concentrations were detected by ELISA. Results After being cultured with Aspergillus fumigatus conidia for 4 and 24 hours, both ICAM-1 and TNF-α secreted in A549 cells significantly increased(P<0.05), compared with control group. Compared with the stimulation of Aspergillus fumigatus conidia alone, 2.5 mg/L azithromycin significantly inhibited the secretion of TNF-α in A549 cells incubated with Aspergillus fumigatus conidia for 24 hours(P<0.05). While, 2.5 mg/L dexamethasone significantly inhibited the secretion of both TNF-α (P<0.05) and ICAM-1 in A549 cells incubated with Aspergillus fumigatus conidia for 24 hours (P<0.05). Conclusion Azithromycin and dexamethasone can inhibit the secretion of ICAM-1 and TNF-α in A549 cells stimulated with Aspergillus fumigatus conidia and thus relieve the inflammatory response of lung.

Key words: Cytokines, Azithromycin, Dexamethasone, Aspergillus fumigatus conidia, A549 cells

中图分类号: 

  • R379.6
[1] 中华内科杂志编委会. 侵袭性肺部真菌感染的诊断标准与治疗原则(草案)[J]. 中华内科杂志, 2006, 45(8):697-702.
[2] Balloy V, Sallenave J M, Wu Y, et al. Aspergillus fumigatus-induced interleukin-8 synthesis by respiratory epithelial cells is controlled by the phosphatidylinositol 3-kinase, p38 MAPK and ERKl/2 pathways and not by the toll-like receptor-MyD88 pathway[J]. J Biol Chem, 2008, 283(45):30513-30521.
[3] Bellanger A P, Millon L, Khonfache K, et al. Aspergilhs fumigatus germ tube growth and not conidia ingestion induces expression of inflammatory mediator genes in the human lung epithelial cell line A549[J]. J Med Microbiol, 2009, 58(part 2):174-179.
[4] Luther K, Rohde M, Heesemann J, et al. Quantification of phagocytosis of Aspergillus conidia by macrophages using a novel antibody-independent assay[J]. J Microbiol Methods, 2006, 66(1):170-173.
[5] Filler S G, Sheppard D C. Fungal invasion of normally non-phagocytic host cells[J]. PLoS Pathog, 2006, 2(12):e129. doi:10.1371/journal.ppat.0020129.
[6] Wasylnka J A, Moore M M. Aspergillus fumigatus conidia survive and germinate in acidic organelles of A549 epithelial cells[J]. J Cell Sci, 2003, 116(part 8):1579-1587.
[7] Berkova N, Lair-Fulleringer S, Femenia F, et al. Aspergillus fumigatus conidia inhibit tumour necrosis factor-or staurosporine-induced apoptosis in epithelial cells[J]. Int Immunol, 2006, 18(1):139-150.
[8] Chotirmall S H, Al-Alawi M, Mirkovic B, et al. Expand+Aspergillus-associated airway disease, inflammation, and the innate immune response[J]. Biomed Res Int, 2013, 2013: 723129. doi:10.1155/2013/723129.
[9] Brieland J K, Jackson C, Menzel F, et al. Cytokine networking in lungs of immunocompetent mice in response to inhaled Aspergillus fumigatus[J]. Infect Immun, 2001, 69(3):1554-1560.
[10] Femenia F, Huet D, Lair-Fulleringer S, et al. Effects of conidia of various Aspergillus species on apoptosis of human pneumocytes and bronchial epithelialcells[J]. Mycopatholoqia, 2009, 167(5):249-262.
[11] Chiang L Y, Sheppard D C, Gravelat F N, et al. Aspergillus fumigatus stimulates leukocyte adhesion molecules and cytokine production by endothelial cells in vitro and during invasive pulmonary disease[J]. Infect Immun, 2008, 76(8):3429-3438.
[12] Zimmermann G S, Neurohr C, Villena-Hermoza H, et al. Anti-inflammatory effects of antibacterials on human bronchial epithelial cells[J]. Respir Res, 2009, 10: 89. doi: 10.1186/1465-9921-10-89.
[13] Cigana C, Assael B M, Melotti P. Azithromycin selectively reduces tumor necrosis factor alpha levels in cystic fibrosis airway epithelial cells[J]. Antimicrob Agents Chemother, 2007, 51(3):975-981.
[1] 黄竹青,吴雪韦,任冬梅. 槲寄生中酚类化学成分的分离鉴定及其对A549细胞的增殖抑制活性[J]. 山东大学学报(医学版), 2017, 55(8): 35-41.
[2] 余桂芳,陈树娣,陈雪竹,侯开连,梁敏. miR-916a调控SOCS6促进HBx-HepG2细胞生长[J]. 山东大学学报(医学版), 2016, 54(12): 14-19.
[3] 袁冰,李冉冉,韩明勇. 恶性黑色素瘤调节肺组织微环境并促进肿瘤肺转移的实验研究[J]. 山东大学学报(医学版), 2016, 54(11): 13-18.
[4] 张明明,安永辉,韩彩莉,张瑛琪,马明,李娜,邹长鹏. CIK细胞联合光动力治疗中晚期食管癌的疗效观察[J]. 山东大学学报(医学版), 2016, 54(1): 38-41.
[5] 李秀华, 李晓丽, 段瑞生, 朱梅佳, 曹莉莉, 李衍滨, 王思, 岳龙涛, 马庆海, 刘菲. 1,25(OH)2D3诱导实验性自身免疫性重症肌无力大鼠免疫耐受的机制[J]. 山东大学学报(医学版), 2015, 53(8): 5-10.
[6] 张蓬, 岳龙涛, 李亨, 张民, 王聪聪, 段瑞生, 窦迎春. 血脂康对实验性自身免疫性神经炎的治疗潜能[J]. 山东大学学报(医学版), 2015, 53(2): 1-5.
[7] 冯青, 谭晓冬. L161982对大鼠实验性自身免疫性神经炎中巨噬细胞亚型变化的影响[J]. 山东大学学报(医学版), 2015, 53(10): 21-25.
[8] 杨永荣, 李俊, 梁烨, 李近都, 蓝家富, 李天资. TNF-α-238G/A基因多态性与口腔扁平苔藓的关系[J]. 山东大学学报(医学版), 2014, 52(S1): 10-11.
[9] 陈国玲, 任然, 张英辉, 宋玮, 考欣, 张晗. 大黄素对角膜炎大鼠角膜组织NF-κB活化表达的影响及意义[J]. 山东大学学报(医学版), 2014, 52(9): 44-47.
[10] 赵燕1,王刚1,陈大方2,程宇航1,陈雪彦1 . 首发未治精神分裂症患者IL-6、IL-10和IL-12水平及影响因素[J]. 山东大学学报(医学版), 2014, 52(4): 70-73.
[11] 隋翔宇, 张相春, 张光永, 胡三元, 王延磊, 戴勇. 连环蛋白p120在炎性肺损伤中保护作用的初步研究[J]. 山东大学学报(医学版), 2014, 52(12): 41-44.
[12] 刘冰1,于壮1,侯宪鹏1,姚如永2. EGFR和HER-3在人肺腺癌细胞及培美曲塞二钠耐药细胞中的表达差异[J]. 山东大学学报(医学版), 2013, 51(5): 20-23.
[13] 刘露1,张雯1,陈翰祥1,郑琳1,卢翌2,王红1,唐伟1,赵蔚明1. PGRN缺失型腹膜巨噬细胞对细菌脂多糖的体外炎症应答[J]. 山东大学学报(医学版), 2013, 51(3): 58-62.
[14] 唐琳娜,吴大玮,杨洁,卢海宁,张帆,韩辉,郭海鹏. 不同剂量地塞米松对脓毒症小鼠肺组织糖皮质激素受体-α表达及肺损伤的影响[J]. 山东大学学报(医学版), 2013, 51(10): 19-23.
[15] 刘庆亮1,牟晓燕1,王静2,迟翔宇2,张敏3,马卫霞3. RNA干扰及厄洛替尼阻断EGFR信号途径对A549细胞抗增殖的影响[J]. 山东大学学报(医学版), 2012, 50(9): 11-.
Viewed
Full text


Abstract

Cited

  Shared   
  Discussed   
No Suggested Reading articles found!