EB病毒感染对慢性阻塞性肺疾病急性加重期炎症反应影响41例临床研究
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摘要
目的研究EB病毒感染对慢性阻塞性肺疾病(慢阻肺)急性加重影响。方法将贵州省人民医院呼吸与危重症医学科2015年10月至2017年8月收治的156慢阻肺急性加重期患者分为EB病毒感染组41例,EB病毒未感染组115例。采用聚合酶链式反应(PCR)检测患者外周血EB病毒DNA,酶联免疫吸附试验(ElISA)检测血清EB抗体IgG、IgM和检测血清中降钙素原(PCT)、C反应蛋白(CRP)、白介素(IL)-6、IL-17、IL-10等表达情况。痰培养和药敏实验分析细菌学特点。分析EB病毒感染患者合并肺部感染常见病原菌特点,对其治疗效果、预后进行综合分析。结果 EB病毒感染的慢阻肺急性加重患者肺部感染血清中的PCT、CRP、IL-6、IL-17、IL-10显著高于非EB病毒感染的慢阻肺急性加重患者,其病原学特点为感染EB病毒患者多为革兰阴性菌所致的肺部感染,且耐药菌比例增加,抗感染治疗时间延长、并发症增加、入住重症病房比例增加。血气方面,感染EB病毒的慢阻肺急性加重患者其PaCO2明显升高,PaO2明显下降,且差异具有统计学意义。而肺功能方面,两组间未见明显差异。结论 EB病毒感染后加重慢阻肺急性加重患者炎症反应程度、促进病情进展与恶化。
Objective To study the effect of Epstein-Barr virus(EB) virus infection on acute exacerbation of chronic obstructive pulmonary disease. Methods 156 patients with acute exacerbation of chronic obstructive pulmonary disease were divided into two groups, 41 patients with EB virus infection and the group 115 patients without EB virus infection.which colleceted from the Department of Respiratory and Critical Care Medicine, Guizhou Provincial People's Hospital From October 2015 to August 2017. Epstein-Barr virus(EB) DNA was detected by PCR, serum EB antibody IgG and IgM were detected by Elisa, and the expression level of PCT, CRP, IL6,IL-17 and IL-10 in serum were detected by Elisa.Sputum culture and sensitivity were used to analyze the bacteriological characteristics. The characteristics of common pathogens of pulmonary infection were also analyzed in patients with Epstein-Barr virus(EBV) infection,and the therapeutic effects and prognosis were analyzed comprehensively. Results The EBV-infected AECOPD patients had significantly higher levels of PCT, CRP and IL-6 IL-17, IL-10 in serum of patients with lung infection than those of AECOPD patients with non-EB virus infection. The etiological characteristics of EBV-infected AECOPD patients were mostly G-, The EBV-infected AECOPD patients whose the proportion of drug-resistant bacteria increased, anti-infective treatment time prolonged, complications increased, admitted to intensive care unit increased. Blood gas, the infection of Epstein-Barr virus AECOPD patients was significantly higher PaCO2, PaO2 decreased significantly, and the difference was statistically significant. However, the lung function, no significant difference between the two groups. Conclusion EBV infection aggravates inflammatory response in patients with AECOPD, and promotes the progress and deterioration of the disease.
Objective To study the effect of Epstein-Barr virus(EB) virus infection on acute exacerbation of chronic obstructive pulmonary disease. Methods 156 patients with acute exacerbation of chronic obstructive pulmonary disease were divided into two groups, 41 patients with EB virus infection and the group 115 patients without EB virus infection.which colleceted from the Department of Respiratory and Critical Care Medicine, Guizhou Provincial People's Hospital From October 2015 to August 2017. Epstein-Barr virus(EB) DNA was detected by PCR, serum EB antibody IgG and IgM were detected by Elisa, and the expression level of PCT, CRP, IL6,IL-17 and IL-10 in serum were detected by Elisa.Sputum culture and sensitivity were used to analyze the bacteriological characteristics. The characteristics of common pathogens of pulmonary infection were also analyzed in patients with Epstein-Barr virus(EBV) infection,and the therapeutic effects and prognosis were analyzed comprehensively. Results The EBV-infected AECOPD patients had significantly higher levels of PCT, CRP and IL-6 IL-17, IL-10 in serum of patients with lung infection than those of AECOPD patients with non-EB virus infection. The etiological characteristics of EBV-infected AECOPD patients were mostly G-, The EBV-infected AECOPD patients whose the proportion of drug-resistant bacteria increased, anti-infective treatment time prolonged, complications increased, admitted to intensive care unit increased. Blood gas, the infection of Epstein-Barr virus AECOPD patients was significantly higher PaCO2, PaO2 decreased significantly, and the difference was statistically significant. However, the lung function, no significant difference between the two groups. Conclusion EBV infection aggravates inflammatory response in patients with AECOPD, and promotes the progress and deterioration of the disease.
引文
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[13]Bektas A, Schurman SH, Sen R, et al. Human T cell immunosenescence and inflammation in aging[J]. J Leukoc Biol, 2017, 102(4):977-988.
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[15]Larsen JM. The immune response to Prevotella bacteria in chronic inflammatory disease[J]. Immunology, 2017, 151(4):363-374.
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[22]SalvoP,DiniV,KirchhainA,etal.SensorsandBiosensorsfor C-Reactive Protein, Temperature and pH, and Their Applications for MonitoringWoundHealing:AReview[J].Sensors(Basel),2017,17(12):pii:E2952.
[23]Smith KJ, Au B, Ollis L, et al. The association between C-reactive protein,Interleukin-6anddepressionamongolderadultsinthe community:A systematic review and meta-analysis[J]. Exp Gerontol,2017, 102:109-132.
[24]Nanke Y, Yago T, Kotake S. The Role of Th17 Cells in the Pathogenesis of Behcet’s Disease[J]. J Clin Med, 2017, 6(7)pii:E74.
[25]Isailovic N, Daigo K, Mantovani A, et al. Interleukin-17 and innate immunity in infections and chronic inflammation[J]. J Autoimmun,2015, 60:1-11.
[26]Patil RS, Bhat SA, Dar AA, et al. The Jekyll and Hyde story of IL17-ProducingγδT Cells[J]. Front Immunol, 2015, 6:37.
[27]Rose-John S, Winthrop K, Calabrese L. The role of IL-6 in host defence against infections:immunobiology and clinical implications[J]. Nat Rev Rheumatol, 2017, 13(7):399-409.
[28]Ma L, Zhang H, Yin YL, et al. Role of interleukin-6 to differentiate sepsisfromnon-infectioussystemicinflammator yresponse syndrome[J]. Cytokine, 2016, 88:126-135.
[29]Zhu L, Shi T, Zhong C, et al. IL-10 and IL-10 Receptor Mutations in Very Early Onset Inflammatory Bowel Disease[J]. Gastroenterol Res,2017, 10(2):65-69.
[30]Rojas JM, Avia M, Martín V, et al. IL-10:A Multifunctional Cytokine in Viral Infections[J]. J Immunol Res, 2017, 2017:6104054.
[31]Vannini F, Kashfi K, Nath N. The dual role of iNOS in cancer[J]. Redox Biol, 2015, 6:334-343.
[32]Rapozzi V, Della Pietra E, Bonavida B. Dual roles of nitric oxide in the regulation of tumor cell response and resistance to photodynamic therapy[J]. Redox Biol, 2015, 6:311-317.
[33]Iwakiri Y, Kim MY. Nitric oxide in liver diseases[J]. Trends Pharmacol Sci, 2015, 36(8):524-536.
[2]Menon MP, Hutchinson L, Garver J, et al. Transformation of follicular lymphoma to Epstein-Barr virus-related Hodgkin-like lymphoma[J]. J Clin Oncol, 2013, 31(5):e53-66.
[3]Yui S, Yamaguchi H, Imadome K, et al. Epstein-Barr Virus-positive T-cell Lymphoproliferative Disease Following Umbilical Cord Blood Transplantation for Acute Myeloid Leukemia[J]. J Nippon Med Sch,2016, 83(1):35-42.
[4]Sun L, Huang M, Wang J, et al. Genotyping of Pneumocystis jirovecii isolatesfromhumanimmunodeficiencyvirus-negativepatientsin China[J]. Infect Genet Evol, 2015, 31:209-215.
[5]LiY,PattanV,SyedB,etal.Splenicinfarctioncausedbyarare coinfection of Epstein-Barr virus, cytomegalovirus, and Mycoplasma pneumoniae[J]. Pediatr Emerg Care, 2014, 30(9):636-647.
[6]KawamotoK,MiyoshiH,SuzukiT,etal.Adistinctsubtypeof Epstein Barr virus positive T/NK-cell lymphoproliferative disorder:Adult patients with chronic active Epstein Barr virus infection-like features[J]. Haematologica, 2018, 103(6):1018-1028.
[7]Stolz D, Hirsch HH, Schilter D, et al. Intensified Therapy with Inhaled Corticosteroids and Long-Actingβ2-Agonists at the Onset of Upper Respiratory Tract Infection to Prevent Chronic Obstructive Pulmonary Disease Exacerbations. A Multicenter, Randomized, Double-Blind,Placebo-controlled Trial[J]. Am J Respir Crit Care Med, 2018, 197(9):1136-1146.
[8]冯学威,李胜岐,郭津津,等.疱疹科病毒潜伏感染与慢性阻塞性肺疾病急性发作的关系[J].中国呼吸与危重监护杂志,2003, 2(3):171-173.
[9]Yao JJ, Zhou GQ, Wang YQ, et al. Prognostic values of the integrated model incorporating the volume of metastatic regional cervical lymph node and pretreatment serum Epstein-Barr virus DNA copy number in predicting distant metastasis in patients with N1 nasopharyngeal carcinoma[J]. Chin J Cancer, 2017, 36(1):98.
[10]冯学威,李胜岐,郭津津,等.疱疹科病毒潜伏感染与慢性阻塞性肺疾病急性发作的关系[J].中国呼吸与危重监护杂志,2003, 2(3):171-173.
[11]李文益,薛红漫. EB病毒感染相关性噬血细胞综合征的发病机制、诊断和治疗[J].中华妇幼临床医学杂志(电子版), 2011,7(2):92-96.
[12]Zhang W, Chen B, Chen Y, et al. Epstein-Barr Virus-Associated Acute Liver Failure Present in a 67-Year-Old Immunocompetent Female[J].Gastroenterol Res, 2016, 9(4-5):74-78.
[13]Bektas A, Schurman SH, Sen R, et al. Human T cell immunosenescence and inflammation in aging[J]. J Leukoc Biol, 2017, 102(4):977-988.
[14]Selmi C. Autoimmunity in 2016[J]. Clin Rev Allergy Immunol, 2017,53(1):126-139.
[15]Larsen JM. The immune response to Prevotella bacteria in chronic inflammatory disease[J]. Immunology, 2017, 151(4):363-374.
[16]NiemanDC,MitmesserSH.PotentialImpactofNutritionon ImmuneSystemRecoveryfromHeavyExertion:AMetabolomics Perspective[J]. Nutrients, 2017, 9(5):E513-522.
[17]Fuentes E, Fuentes M, Palomo I. ImmuneSystemDysfunction in the Elderly[J]. An Acad Bras Cienc, 2017, 89(1):285-299.
[18]Levin BR, Baquero F, Ankomah PP, et al.Phagocytes, Antibiotics, and Self-Limiting Bacterial Infections[J]. Trends Microbiol, 2017, 25(11):878-892.
[19]SamsudinI,VasikaranSD.ClinicalUtilityandMeasurementof Procalcitonin[J]. Clin Biochem Rev, 2017, 38(2):59-68.
[20]LippiG,Sanchis-GomarF.Procalcitoninininflammatorybowel disease:Drawbacks and opportunities[J]. World J Gastroenterol, 2017,23(47):8283-8290.
[21]Vijayan AL, Vanimaya, Ravindran S, et al. Procalcitonin:a promising diagnostic marker for sepsis and antibiotic therapy[J]. J Intensive Care.2017, 5:51.
[22]SalvoP,DiniV,KirchhainA,etal.SensorsandBiosensorsfor C-Reactive Protein, Temperature and pH, and Their Applications for MonitoringWoundHealing:AReview[J].Sensors(Basel),2017,17(12):pii:E2952.
[23]Smith KJ, Au B, Ollis L, et al. The association between C-reactive protein,Interleukin-6anddepressionamongolderadultsinthe community:A systematic review and meta-analysis[J]. Exp Gerontol,2017, 102:109-132.
[24]Nanke Y, Yago T, Kotake S. The Role of Th17 Cells in the Pathogenesis of Behcet’s Disease[J]. J Clin Med, 2017, 6(7)pii:E74.
[25]Isailovic N, Daigo K, Mantovani A, et al. Interleukin-17 and innate immunity in infections and chronic inflammation[J]. J Autoimmun,2015, 60:1-11.
[26]Patil RS, Bhat SA, Dar AA, et al. The Jekyll and Hyde story of IL17-ProducingγδT Cells[J]. Front Immunol, 2015, 6:37.
[27]Rose-John S, Winthrop K, Calabrese L. The role of IL-6 in host defence against infections:immunobiology and clinical implications[J]. Nat Rev Rheumatol, 2017, 13(7):399-409.
[28]Ma L, Zhang H, Yin YL, et al. Role of interleukin-6 to differentiate sepsisfromnon-infectioussystemicinflammator yresponse syndrome[J]. Cytokine, 2016, 88:126-135.
[29]Zhu L, Shi T, Zhong C, et al. IL-10 and IL-10 Receptor Mutations in Very Early Onset Inflammatory Bowel Disease[J]. Gastroenterol Res,2017, 10(2):65-69.
[30]Rojas JM, Avia M, Martín V, et al. IL-10:A Multifunctional Cytokine in Viral Infections[J]. J Immunol Res, 2017, 2017:6104054.
[31]Vannini F, Kashfi K, Nath N. The dual role of iNOS in cancer[J]. Redox Biol, 2015, 6:334-343.
[32]Rapozzi V, Della Pietra E, Bonavida B. Dual roles of nitric oxide in the regulation of tumor cell response and resistance to photodynamic therapy[J]. Redox Biol, 2015, 6:311-317.
[33]Iwakiri Y, Kim MY. Nitric oxide in liver diseases[J]. Trends Pharmacol Sci, 2015, 36(8):524-536.