期刊文献+

髓系细胞触发受体-1在输血相关性急性肺损伤大鼠肺组织的表达 被引量:3

Myeloid cell triggering receptor 1 expression related acute lung injury in rat lung tissue in blood transfusions
原文传递
导出
摘要 目的观察髓系细胞触发受体(TREM-1)在输血相关性急性肺损伤(TRALI)SpragueDawley(SD)大鼠肺组织中的表达及其在TRALI发病机理中的作用。方法sD大鼠55只,随机分为TRALI组(n=25)、正常对照组(n=10)和阳性对照组(n=20)。TRALI组腹腔注射脂多糖(LPS)2mg/kg2h后静脉输注人血浆(1ml/只);正常对照组腹腔注射生理盐水2mg/kg,移除1mJ大鼠血液后及时输注等体积生理盐水;阳性对照组静脉输注LPS5mg/kg诱导急性肺损伤。3组分别于造模后6h留取外周血及肺组织,采用荧光实时定量反转录多聚酶链反应法(RT-PCR)检测大鼠外周血及肺组织TREM-1mRNA;酶联免疫吸附试验(ELISA)检测大鼠外周血及肺组织TREM-1和肿瘤坏死因子(TNF)-α浓度;HE染色进行大鼠肺组织Smith病理损伤评分。Spearman相关性分析TRALI组TREM-1mRNA、TNF-α和Smith病理损伤评分3者之间的相关性。结果TRALI组和阳性对照组大鼠肺组织TREM-1mRNA的表达(4.96±0.08、6.35±0.09)高于正常对照组(1.01±0.00)(均P〈0.05),血TREM-1mRNA的表达(9.85±3.23、12.33±3.56)也高于正常对照组(2.15±0.35)(均P〈0.05)。TRALI组大鼠肺组织和血TREM-1浓度[(695.25±116.87)、(703.80±100.67)ng/L]高于正常对照组[(234.51±44.38)、(240.22±46.63)ng/L](均P〈0.05),但与阳性对照组差异无统计学意义(均P〉0.05)。TRALI组大鼠肺组织和血TNF-α浓度[(288.26±35.53)、(276.26±39.53)ng/L]显著高于正常对照组[(216.34±33.45)、(220.60±38.30)ng/L](均P〈0.05),但与阳性对照组差异无统计学意义(均P〉0.05)。TRALI组Smith病理损伤评分(7.46±0.95)显著高于正常对照组(0.32±0.28)(P〈0.05),与阳性对照组(8.65±0.72)差异无统计学意义(P〉0.05)。TRALI组大鼠肺组织Smith病理损伤评分与肺组织TREM-1mRNA表达及浓度、TNF-α浓度呈正相关(r=0.377、0.489、0.763,均P〈0.05),肺组织TREM-1mRNA表达与肺组织TNF-α浓度无相关性(P〉0.05),但TREM-1浓度与TNF-α浓度正相关(r=0.689,P〈0.05)。结论TRALI大鼠肺组织中TREM-1浓度升高,与TNF-α浓度及肺损伤程度相关,提示TREM-1可能参与了TRALI肺部炎性反应。 Objective To investigate the expression of trigger receptors on myeloid cells (TREM- 1 ) in lung tissue of Sprague Dawley (SD) rats with transfusion-related acute lung injury (TRALI) and its role in the pathogenesis of TRALI. Methods Fifty-five SD rats were randomly divided into TRALI group (n= 25) , normal control group (n=10) and the positive control group (n=20). The TRALI group was given intraperitoneal injection of 2 mg/kg lipopolysaccharide (LPS) followed by intravenous infusion of human plasma (1 murat) at 2 h later; the normal control group was intraperitoneal injection of 2 mg/kg saline, followed by intravenous infusion of 1 ml saline after withdrawal of 1 ml blood; the positive control group was given intravenously 5 mg/kg LPS to induce lung injury. At 6 h after modeling, the rats in the three groups were collected of peripheral blood and harvested for lung tissue specimens. Real-time quantitative reverse transcription polymerase chain reaction (RT- PCR) was used to detect the TREM- 1 mRNA in the rat peripheral blood and lung tissue. ELISA assay was employed to measure the levels of TREM- 1 and tumor necrosis factor (TNF)- ct in the rat peripheral blood and lung tissue. HE staining of rat lung tissue was performed for Smith pathological scoring. Spearman correlation analysis was performed to determine the correlation among TREM-1 mRNA, TNF-a and Smith pathological scores in the TRALI group. Results The expression of TREM-1 mRNA in rat lung tissue of the TRALI group (4.96±0.08) and positive control group (6.35_+0.09) was higher than that in the control group (1.01±0.00) (all P〈0.05 ), and so was the expression of TREM-1 mRNA in rat peripheral blood of the TRALI group (9.85 ±3.23) and positive control group (12.33±3.56) compared with the control group (2.15±0.35) Call P〈0.05). TREM-1 concentrations in the lung tissue and blood of TRALI group [ (695.25± 116.87) and (703.80± 100.67) ng/Ll were higher than those in the control group [ (234.51±44.38) and (240.22±46.63) ng/L] (all P〈0.05) , but were not statistically different from those in the positive control group (P〉0.05). TNF-α concentrations in the lung tissue and blood of TRALI group [ (288.26±35.53) and (276.26±39.53) ng/L] were higher than those in the control group [ (216.34±33.45) and (220.60±38.30) ng/L] (all P〈0.05), but were not statistically different from those in the positive control group (P〉0.05). The Smith pathological score in the TRALI group (7.46±0.95) was significantly higher than that in the control group (0.32±0.28) (P〈0.05), but was not statistically different from that in the positive control group (8.65_+0.72) (P〉0.05). In the TRALI group, Smith pathological score was positively correlated with TREM-1 mRNA expression (r=0.377), TREM-1 (r= 0.489) and TNF-α (r=0.763) concentrations in rat lung tissue (all P〈0.05) ; lung tissue TREM- 1 concentration (r=0.689, P〈0.05), but not TREM-1 mRNA expression, was correlated with lung tissue TNF- a concentration. Conclusion TREM- 1 concentration is elevated in lung tissue of rats with TRALI and correlated with lung TNF-α level and severity of lung injury, suggesting that TREM-1 may be involved in the inflammatory response in lung TRALI.
出处 《中华生物医学工程杂志》 CAS 2015年第5期417-421,共5页 Chinese Journal of Biomedical Engineering
关键词 急性肺损伤 髓系细胞触发受体-1 肿瘤坏死因子Α 病理评分 Acute lung injury Triggering receptor-1 expressed on myeloid cells Tumornecrosis factor-alpha Pathology score
  • 相关文献

参考文献21

  • 1Kenz P, Van der Linden P. Transfusion-related acute lung injury [J]. Eur J Anaesthesiol, 2014, 31(7) : 345-350.
  • 2Chapman CE, Stainsby D, Jones H, et al. Ten years of hemovigilance reports of transfusion-related acute lung injury in the United Kingdom and the impact of preferential use of male donor plasma [J]. Transfusion, 2008, 49(3) : 440-452.
  • 3廖刃,刘进.围手术期血液管理:由限制性输血走向个体化输血[J].中华医学杂志,2014,94(7):481-482. 被引量:47
  • 4Bouchon A, Dietrich J, Colonna M. Cutting edge: inflammatory responses can be triggered by TREM- 1, a novel receptor expressed on neutrophils and monocytes [J]. J Immunol, 2000, 164(10) : 4991-4995.
  • 5Bouchon A, Faechetti F, Weigand MA, et al. TREM-I amplifies inflammation and is a crucial mediator of septic shock J]. Nature, 2001,410(6832) : 1103-1107.
  • 6Silliman CC. The two-event model of transfusion-related acute lung injury[J]. Cri t Care Med, 2006, 34(5 Suppl) : S124-131.
  • 7Nicholson SE, Johnson RA, Craig T, et al. Transfusion-related acute lung injury in a rat model of trauma-hemorrhage [J]. J Trauma, 2011, 70(2): 466-471.
  • 8Kelher MR, Masuno T, Moore EE, et al. Plasma from storedpacked red blood cells and MHC class I antibodies causes acute lung injury in a 2-event in vivo rat model[J]. Blood, 2009, 113 (9) : 2079-2087.
  • 9Hashimoto N, Kawabe T, Imaizumi K, et al. CD40 plays a crucial role in lipopolysaccharide-induced acute lung injury [J]. AM J Respir Cell Mol Biol, 2004, 30(6) : 808-815.
  • 10佟欣,栾婷,李国福,臧彬.早期抗凝对脂多糖致急性肺损伤大鼠的保护作用[J].中华危重病急救医学,2014,26(11):836-838. 被引量:5

二级参考文献48

  • 1雷文章,韦靖江,沈文律,金立人.实验性坏死性胰腺炎多器官损害与内毒素血症的关系[J].中华实验外科杂志,1995,12(3):131-132. 被引量:117
  • 2李海东,游斌,刘国祥.LPS诱导急性肺损伤大鼠肺组织甲状腺转录因子-1表达变化[J].中国急救医学,2005,25(11):810-812. 被引量:3
  • 3蒋飞,范红.Fas/FasL系统在急性肺损伤致病机制中的研究进展[J].中国呼吸与危重监护杂志,2007,6(2):145-147. 被引量:2
  • 4Ashbaugh DG,Bigelow DB,Petty TL,et al.Acute respiratory distress in adults[J].Lancet,1967,2 (7511):319-223.
  • 5Ware LB,Matthay MA.The acute respiratory distress syndrome[J].N Engl J Med,2000,342 (18):1334-1349.
  • 6Martin C,Papazian L,Payan MJ,et al.Pulmonary fibrosis correlates with outcome in adult respiratory distress syndrome.A study in mechanically ventilated patients[J].Chest,1995,107 (1):196-200.
  • 7Fernandes AB,Zin WA,Rocco PR.Corticosteroids in acute respiratory distress syndrome[J].Braz J Med Biol Res,2005,38(2):147-159.
  • 8Meduri GU,Headley AS,Golden E,et al.Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome:a randomized controlled trial[J].JAMA,1998,280(2):159-165.
  • 9AnnaneD,Sebille V,Bellissant E.Effect of low doses of corticosteroids in septic shock patients with or without early acute respiratory distress syndrome[J].Crit Care Med,2006,34 (1):22-30.
  • 10Kesecioglu J,Haitsma JJ.Surfactant therapy in adults with acute lung injury/acute respiratory distress syndrome[J].Curr Opin Crit Care,2006,12 (1):55-60.

共引文献90

同被引文献23

引证文献3

二级引证文献16

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部