doi:

DOI: 10.3724/SP.J.1008.2015.01284

Academic Journal of Second Military Medical University (第二军医大学学报) 2015/36:12 PP.1284-1288

Aggravated airway inflammation and resistance in a respiratory syncytial virus infected murine asthma model


Abstract:
Objective To explore the role of respiratory syncytial virus (RSV) infection in aggravating airway inflammation and airway resistance in murine asthma model. Methods A total of 30 6-8-week-old male BALB/c mice were equally divided into three groups randomly: the control group, ovalbumin (OVA) group (asthma group), and respiratory syncytial virus (RSV)/OVA group (RSV+asthma group). In OVA group, murine asthma model was established using an OVA sensitization; in OSV/RSV group, mice were firstly sensitized by OVA and subsequently infected with RSV intranasally for three times to make acute viral infection asthma model; and in control group, the mice received equal volume of PBS treatment. Twenty-four hours after the last challenge, the airway resistance was evaluated by mouse ventilator (Buxco RC). Inflammatory cell infiltration was measured in bronchoalveolar lavage fluid (BALF). Pulmonary tissue samples were collected and stained with H-E, PAS or VG to observe inflammation of pulmonary tissues. Results Pulmonary tissue of mice in OVA group had inflammatory cell infiltration, airway mucus secretions were visible, and collagen was seen around the airway. Pulmonary tissue of mice in OVA/RSV group had significant inflammatory cell infiltration, alveolar stenosis, telangiectasia congestion, airway mucus secretions and collagen deposition. Lung function and the proportion of BALF eosinophils (EOS%) in OVA group and OVA/RSV group were significantly different from that of the control group (P<0.05,P<0.01). Airway resistance and the EOS% in OVA/RSV group were significantly different from those of the OVA group (P<0.05). Conclusion RSV infection can aggravate the airway inflammation and result in airway resistance in murine asthma model.

Key words:respiratory syncytial viruses;asthma;airway inflammation;airway resistance

ReleaseDate:2016-05-27 09:19:59



[1] Kumar A, Grayson M H. The role of viruses in the development and exacerbation of atopic disease[J]. Ann Allergy Asthma Immunol, 2009, 103:181-186.

[2] Hacking D, Hull J. Respiratory syneytial virus-viral biology and the host response[J].J Infect, 2002, 45:18-24.

[3] Newcomb D C, Boswell M G, Reiss S, Zhou W, Goleniewska K, Toki S, et al. IL-17A inhibits airway reactivity induced by respiratory syncytial virus infection during allergic airway inflammation[J]. Thorax, 2013, 68:717-723.

[4] Krishnamoorthy N, Khare A, Oriss T B, Raundhal M, Morse C, Yarlagadda M, et al. Early infection with respiratory syncytial virus impairs regulatory T cell function and increases susceptibility to allergic asthma[J]. Nat Med, 2012, 18:1525-1530.

[5] Aeffner F, Davis I C. Respiratory syncytial virus reverses airway hyperresponsiveness to methacholine in ovalbumin-sensitized mice[J]. PLoS One, 2012, 7:e46660.

[6] 臧 娜, 王莉佳, 陈伟超, 谢晓虹, 邓 旻, 刘恩梅, 等.呼吸道合胞病毒空斑检测方法的建立及应用[J].中国生物制品学杂志, 2010, 23:192-195.

[7] Sun J, Li L, Wu J, Liu B, Gong W, Lv Y, et al. Effects of baicalin on airway remodeling in asthmatic mice[J].Planta Med, 2013, 79(3-4):199-206.

[8] 尚云晓, 冯 雍.2014版全球哮喘防治创议(GINA)解读--与儿童哮喘相关内容[J].中国实用儿科杂志, 2014, 29:669-672.

[9] Global Initiative for Asthma. Pocket guide for asthma management and prevention[EB/OL].(2012-12)[2013-05-25]http://www.ginasthma.org/local/uploads/files/GINA_Pocket_2013_May 15.pdf.

[10] Global Initiative for Asthma. Global strategy for the diagnosis and management of asthma in children 5 years and younger[EB/OL]. [2013-05-25]. http://www.ginasthnla.org/local/uploads/files/GINA_ Under5_ 2009_ Corx-Augl 1_1.pdf.

[11] 全国儿科哮喘协作组.全国90万0~14岁儿童中支气管患病情况调查[J].中华结核和呼吸杂志, 1993, 16(增刊):64-68.

[12] 全国儿童哮喘防治协作组.中国城区儿童哮喘患病率调查[J].中华儿科杂志, 2003, 41:123-127.

[13] 全国儿科哮喘协作组.2000年与1990年儿童支气管哮喘患病率的调查比较[J].中华结核和呼吸杂志, 2004, 27:112-116.

[14] 全国儿科哮喘协作组, 中国疾病预防控制中心环境与健康相关产品安全所.第三次中国城市儿童哮喘流行病学调查[J].中华儿科杂志, 2013, 51:729-735.

[15] Black C P. Systematic review of the biology and medical management of respiratory syncytial virus infection[J]. Respir Care, 2003, 48:209-233.

[16] Simes E A. RSV disease in the pediatric population: epidemiology, seasonal variability, and long-term outcomes[J]. Manag Care, 2008, 17(11 Suppl 12):3-6, 18-19.

[17] 吴让琼, 陈宇宁.儿童哮喘发作与呼吸道合胞病毒感染关系研究[J].国际病毒学杂志, 2014, 21:277-279.

[18] Gibson P G, Dolovich J, Denburg J, Ramsdale E H, Hargreave F E.Chronic cough: eosinophilic bronchitis without asthm[J]. Lancet, 1989, 1:1346-1348.

[19] 沈 潞, 赖克方, 姜 华, 洪燕华, 钟南山.不同激发方式对小鼠过敏性支气管哮喘模型的影响[J].中华哮喘杂志(电子版), 2009, 3:404-408.

[20] Locke N R, Royce S G, Wainewright J S, Samuel C S, Tang M L.Comparison of airway remodeling in acute, subacute, and chronic models of allergic airways disease[J].Am J Respir Cell Mol Biol, 2007, 36:625-632.

[21] Trujillo-Vargas C M, Werner-Klein M, Wohlleben G, Polte T, Hansen G, Ehlers S, et al. Helminth-derived products inhibit the development of allergic responses in mice[J].Am J Respir Crit Care Med, 2007, 175:336-344.

[22] Ju Y, Choi S J, Lee H, Kim H S, Won S, Chun Y H, et al. Effect of respiratory syncytial virus infection on regulated on activation, normal T-cells expressed and secreted production in a murine model of asthma[J].Korean J Pediatr, 2011, 54:456-462.