請用此 Handle URI 來引用此文件：
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/67725完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 周祖述(Tzuu-Shuh Jou) | |
| dc.contributor.author | Chia-Hsiung Liu | en |
| dc.contributor.author | 柳嘉雄 | zh_TW |
| dc.date.accessioned | 2021-06-17T01:46:16Z | - |
| dc.date.available | 2020-09-12 | |
| dc.date.copyright | 2017-09-12 | |
| dc.date.issued | 2017 | |
| dc.date.submitted | 2017-07-27 | |
| dc.identifier.citation | Adamzik, M., Broll, J., Steinmann, J., Westendorf, A. M., Rehfeld, I., Kreissig, C., et al. (2013). An increased alveolar CD4+CD25+Foxp3+ T-regulatory cell ratio in acute respiratory distress syndrome is associated with increased 30-day mortality. Intensive Care Med 39 (10): 1743-1751.
Adib-Conquy, M. and Cavaillon, J. M. (2009). Compensatory anti-inflammatory response syndrome. Thromb Haemost 101 (1): 36-47. Akira S, and Takeda K. (2004). Toll-like receptor signalling. Nat. Rev. Immunol 4 (7): 499–511. Akira S, Uematsu S, and Takeuchi O. (2006). Pathogen recognition and innate immunity. Cell 124 (4): 783–801. Aksoy E, Taboubi S, Torres D, Delbauve S, Hachani A, Whitehead MA, et al. (2012). The p110delta isoform of the kinase PI(3)K controls the subcellular compartmentalization of TLR4 signaling and protects from endotoxic shock. Nat Immunol 13 (11):1045–54. Allavena, P., Piemonti, L., Longoni, D., Bernasconi, S., Stoppacciaro, A., Ruco, L., et al. (1998). IL-10 prevents the differentiation of monocytes to dendritic cells but promotes their maturation to macrophages. Eur J Immunol 28 (1): 359-369. Allen, M. L., Hoschtitzky, J. A., Peters, M. J., Elliott, M., Goldman, A., James, I., et al. (2006). Interleukin-10 and its role in clinical immunoparalysis following pediatric cardiac surgery. Crit Care Med 34 (10): 2658-2665. Amat, M., Barcons, M., Mancebo, J., Mateo, J., Oliver, A., Mayoral, J. F., et al. (2000). Evolution of leukotriene B4, peptide leukotrienes, and interleukin-8 plasma concentrations in patients at risk of acute respiratory distress syndrome and with acute respiratory distress syndrome: mortality prognostic study. Crit Care Med 28 (1): 57-62. Andrassy, M., Volz, H. C., Igwe, J. C., Funke, B., Eichberger, S. N., Kaya, Z., et al. (2008). High-mobility group box-1 in ischemia-reperfusion injury of the heart. Circulation 117 (25): 3216-3226. Aokage, T., Palmer, K., Ichiba, S. and Takeda, S. (2015). Extracorporeal membrane oxygenation for acute respiratory distress syndrome. J Intensive Care 3: 17. Arslan, F., Keogh, B., McGuirk, P. and Parker, A. E. (2010). TLR2 and TLR4 in ischemia reperfusion injury. Mediators Inflamm 2010: 704202. Arumugam, T. V., Okun, E., Tang, S. C., Thundyil, J., Taylor, S. M. and Woodruff, T. M. (2009). Toll-like receptors in ischemia-reperfusion injury. Shock 32 (1): 4-16. Asea, A., Rehli, M., Kabingu, E., Boch, J. A., Bare, O., Auron, P. E., et al. (2002). Novel signal transduction pathway utilized by extracellular HSP70: role of toll-like receptor (TLR) 2 and TLR4. J Biol Chem 277 (17): 15028-15034. Bellani, G., Laffey, J. G., Pham, T., Fan, E., Brochard, L., Esteban, A., et al. (2016). Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries. JAMA 315 (8): 788-800. Beurskens, C. J., Horn, J., de Boer, A. M., Schultz, M. J., van Leeuwen, E. M., Vroom, M. B., et al. (2014). Cardiac arrest patients have an impaired immune response, which is not influenced by induced hypothermia. Crit Care 18 (4): R162. Bhatia, M. and Moochhala, S. (2004). Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome. J Pathol 202 (2): 145-156. Brunialti, M. K., Martins, P. S., Barbosa de Carvalho, H., Machado, F. R., Barbosa, L. M. and Salomao, R. (2006). TLR2, TLR4, CD14, CD11B, and CD11C expressions on monocytes surface and cytokine production in patients with sepsis, severe sepsis, and septic shock. Shock 25 (4): 351-357. Carden, D. L. and Granger, D. N. (2000). Pathophysiology of ischaemia-reperfusion injury. J Pathol 190 (3): 255-266. Castellheim, A., Brekke, O. L., Espevik, T., Harboe, M. and Mollnes, T. E. (2009). Innate immune responses to danger signals in systemic inflammatory response syndrome and sepsis. Scand J Immunol 69 (6): 479-491. Chang, J. W., Lee, S. H., Jeong, J. Y., Chae, H. Z., Kim, Y. C., Park, Z. Y., et al. (2005). Peroxiredoxin-I is an autoimmunogenic tumor antigen in non-small cell lung cancer. FEBS Lett 579 (13): 2873-2877. Chang, J. W., Lee, S. H., Lu, Y. and Yoo, Y. J. (2006). Transforming growth factor-beta1 induces the non-classical secretion of peroxiredoxin-I in A549 cells. Biochem Biophys Res Commun 345 (1): 118-123. Checconi, P., Salzano, S., Bowler, L., Mullen, L., Mengozzi, M., Hanschmann, E. M., et al. (2015). Redox proteomics of the inflammatory secretome identifies a common set of redoxins and other glutathionylated proteins released in inflammation, influenza virus infection and oxidative stress. PLoS One 10 (5): e0127086. Chen, W. and Ware, L. B. (2015). Prognostic factors in the acute respiratory distress syndrome. Clin Transl Med 4 (1): 65. Chen, Y. S., Lin, J. W., Yu, H. Y., Ko, W. J., Jerng, J. S., Chang, W. T., et al. (2008). Cardiopulmonary resuscitation with assisted extracorporeal life-support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and propensity analysis. Lancet 372 (9638): 554-561. Cheng, H. H., Chang, C. S., Wang, H. J. and Wang, W. C. (2010). Interleukin-1beta and -10 polymorphisms influence erosive reflux esophagitis and gastritis in Taiwanese patients. J Gastroenterol Hepatol 25 (8): 1443-1451. Chung, E. Y., Liu, J., Zhang, Y. and Ma, X. (2007). Differential expression in lupus-associated IL-10 promoter single-nucleotide polymorphisms is mediated by poly(ADP-ribose) polymerase-1. Genes Immun 8 (7): 577-589. Clark, J. B., Wang, S., Palanzo, D. A., Wise, R., Baer, L. D., Brehm, C., et al. (2015). Current Techniques and Outcomes in Extracorporeal Life Support. Artif Organs 39 (11): 926-930. Combes, A., Brechot, N., Luyt, C. E. and Schmidt, M. (2012). What is the niche for extracorporeal membrane oxygenation in severe acute respiratory distress syndrome? Curr Opin Crit Care 18 (5): 527-532. Couper, K. N., Blount, D. G. and Riley, E. M. (2008). IL-10: the master regulator of immunity to infection. J Immunol 180 (9): 5771-5777. Davies, A., Jones, D., Bailey, M., Beca, J., Bellomo, R., Blackwell, N., et al. (2009). Extracorporeal membrane oxygenation for 2009 Influenza A(H1N1) acute respiratory distress syndrome. JAMA 302 (17): 1888-1895. Delirezh, N., Shojaeefar, E., Parvin, P. and Asadi, B. (2013). Comparison the effects of two monocyte isolation methods, plastic adherence and magnetic activated cell sorting methods, on phagocytic activity of generated dendritic cells. Cell J 15 (3): 218-223. Edwards-Smith, C. J., Jonsson, J. R., Purdie, D. M., Bansal, A., Shorthouse, C. and Powell, E. E. (1999). Interleukin-10 promoter polymorphism predicts initial response of chronic hepatitis C to interferon alfa. Hepatology 30 (2): 526-530. Enger, T., Philipp, A., Videm, V., Lubnow, M., Wahba, A., Fischer, M., et al. (2014). Prediction of mortality in adult patients with severe acute lung failure receiving veno-venous extracorporeal membrane oxygenation: a prospective observational study. Crit Care 18 (2): R67. Fu, L. H., Ma, C. L., Cong, B., Li, S. J., Chen, H. Y. and Zhang, J. G. (2011). Hypomethylation of proximal CpG motif of interleukin-10 promoter regulates its expression in human rheumatoid arthritis. Acta Pharmacol Sin 32 (11): 1373-1380. Furuta, T., Imajo-Ohmi, S., Fukuda, H., Kano, S., Miyake, K. and Watanabe, N. (2008). Mast cell-mediated immune responses through IgE antibody and Toll-like receptor 4 by malarial peroxiredoxin. Eur J Immunol 38 (5): 1341-1350. Gallagher, P. M., Lowe, G., Fitzgerald, T., Bella, A., Greene, C. M., McElvaney, N. G., et al. (2003). Association of IL-10 polymorphism with severity of illness in community acquired pneumonia. Thorax 58 (2): 154-156. Golovkin, A. S., Matveeva, V. G., Kudryavtsev, I. V., Chernova, M. N., Bayrakova, Y. V., Shukevich, D. L., et al. (2013). Perioperative Dynamics of TLR2, TLR4, and TREM-1 Expression in Monocyte Subpopulations in the Setting of On-Pump Coronary Artery Bypass Surgery. ISRN Inflamm 2013: 817901. Gong, M. N., Thompson, B. T., Williams, P. L., Zhou, W., Wang, M. Z., Pothier, L., et al. (2006). Interleukin-10 polymorphism in position -1082 and acute respiratory distress syndrome. Eur Respir J 27 (4): 674-681. Gray, B. W., Haft, J. W., Hirsch, J. C., Annich, G. M., Hirschl, R. B. and Bartlett, R. H. (2015). Extracorporeal life support: experience with 2,000 patients. Asaio J 61(1): 2-7. Guo, J., He, Y. H., Chen, F., Jiang, M. H., Gao, S. P., Su, Y. M., et al. (2012). The A to G polymorphism at -1082 of the interleukin-10 gene is rare in the Han Chinese population. Mol Med Rep 6 (4): 894-896. Hamers, L., Kox, M. and Pickkers, P. (2015). Sepsis-induced immunoparalysis: mechanisms, markers, and treatment options. Minerva Anestesiol 81 (4): 426-439. Hong, T.-H., Hu, F.-C., Kuo, S.-W., Ko, W.-J., Chow, L.-P., Hsu, L.-M., et al. Predicting outcome in patients under extracorporeal membrane oxygenation due to cardiogenic shock through dynamic change of lymphocytes and interleukins. IJC Metabolic & Endocrine 7: 36-44. Hsin, C. H., Wu, M. Y., Huang, C. C., Kao, K. C. and Lin, P. J. (2016). Venovenous extracorporeal membrane oxygenation in adult respiratory failure: Scores for mortality prediction. Medicine (Baltimore) 95 (25): e3989. Hsu, C. P., Lee, W. C., Wei, H. M., Sung, S. H., Huang, C. Y., Shih, C. C., et al. (2015). Extracorporeal membrane oxygenation use, expenditure, and outcomes in Taiwan from 2000 to 2010. J Epidemiol 25 (4): 321-331. Hubmayr, R. D. and Farmer, J. C. (2010). Should we 'rescue' patients with 2009 influenza A(H1N1) and lung injury from conventional mechanical ventilation? Chest 137 (4): 745-747. Husebye, H., Halaas, O., Stenmark, H., Tunheim, G., Sandanger, O., Bogen, B., et al. (2006). Endocytic pathways regulate Toll-like receptor 4 signaling and link innate and adaptive immunity. Embo J 25 (4): 683-692. Ishii, T., Warabi, E. and Yanagawa, T. (2012). Novel roles of peroxiredoxins in inflammation, cancer and innate immunity. J Clin Biochem Nutr 50 (2): 91-105. Iyer, S. S. and Cheng, G. (2012). Role of interleukin 10 transcriptional regulation in inflammation and autoimmune disease. Crit Rev Immunol 32 (1): 23-63. Jacquet, S., Yin, X., Sicard, P., Clark, J., Kanaganayagam, G. S., Mayr, M., et al. (2009). Identification of cardiac myosin-binding protein C as a candidate biomarker of myocardial infarction by proteomics analysis. Mol Cell Proteomics 8 (12): 2687-2699. Kaczorowski, D. J., Tsung, A. and Billiar, T. R. (2009). Innate immune mechanisms in ischemia/reperfusion. Front Biosci (Elite Ed) 1: 91-98. Kang, X., Kim, H. J., Ramirez, M., Salameh, S. and Ma, X. (2010). The septic shock-associated IL-10 -1082 A > G polymorphism mediates allele-specific transcription via poly(ADP-Ribose) polymerase 1 in macrophages engulfing apoptotic cells. J Immunol 184 (7): 3718-3724. Katakura, T., Miyazaki, M., Kobayashi, M., Herndon, D. N. and Suzuki, F. (2004). CCL17 and IL-10 as effectors that enable alternatively activated macrophages to inhibit the generation of classically activated macrophages. J Immunol 172 (3): 1407-1413. Kearse, M., Moir, R., Wilson, A., Stones-Havas, S., Cheung, M., Sturrock, S., et al. (2012). Geneious Basic: an integrated and extendable desktop software platform for the organization and analysis of sequence data. Bioinformatics 28 (12): 1647-1649. Khalid, L. and Dhakam, S. H. (2008). A review of cardiogenic shock in acute myocardial infarction. Curr Cardiol Rev 4 (1): 34-40. Kim, S., Kim, S. Y., Pribis, J. P., Lotze, M., Mollen, K. P., Shapiro, R., et al. (2013). Signaling of high mobility group box 1 (HMGB1) through toll-like receptor 4 in macrophages requires CD14. Mol Med 19 (1): 88-98. Kim, Y. J., Ahn, J. Y., Liang, P., Ip, C., Zhang, Y. and Park, Y. M. (2007). Human prx1 gene is a target of Nrf2 and is up-regulated by hypoxia/reoxygenation: implication to tumor biology. Cancer Res 67 (2): 546-554. Klinzing, S., Wenger, U., Steiger, P., Starck, C. T., Wilhelm, M., Schuepbach, R. A., et al. (2015). External validation of scores proposed for estimation of survival probability of patients with severe adult respiratory distress syndrome undergoing extracorporeal membrane oxygenation therapy: a retrospective study. Crit Care 19 (1): 142. Koressaar, T. and Remm, M. (2007). Enhancements and modifications of primer design program Primer3. Bioinformatics 23 (10): 1289-1291. Kuok, C. M., Tsao, P. N., Chen, C. Y., Chou, H. C., Hsieh, W. S., Huang, S. C., et al. (2017). Extracorporeal membrane oxygenation support in neonates: a single medical center experience in Taiwan. Pediatr Neonatol. doi: 10.1016/j.pedneo.2016.08.009. [Epub ahead of print] Larsson, L., Rymo, L. and Berglundh, T. (2010). Sp1 binds to the G allele of the-1087 polymorphism in the IL-10 promoter and promotes IL-10 mRNA transcription and protein production. Genes Immun 11 (2): 181-187. Latz, E., Visintin, A., Lien, E., Fitzgerald, K. A., Monks, B. G., Kurt-Jones, E. A., et al. (2002). Lipopolysaccharide rapidly traffics to and from the Golgi apparatus with the toll-like receptor 4-MD-2-CD14 complex in a process that is distinct from the initiation of signal transduction. J Biol Chem 277 (49): 47834-47843. Leentjens, J., Kox, M., van der Hoeven, J. G., Netea, M. G. and Pickkers, P. (2013). Immunotherapy for the adjunctive treatment of sepsis: from immunosuppression to immunostimulation. Time for a paradigm change? Am J Respir Crit Care Med 187 (12): 1287-1293. Lewandowski, K. (2000). Extracorporeal membrane oxygenation for severe acute respiratory failure. Crit Care 4 (3): 156-168. Li, J., Lee, D. S. W., and Madrenas, J. (2013). Evolving bacterial envelopes and plasticity of TLR2-dependent responses: basic research and translational opportunities. Front Immunol 4: 347. Lin, S. Y., Hsieh, S. C., Lin, Y. C., Lee, C. N., Tsai, M. H., Lai, L. C., et al. (2012). A whole genome methylation analysis of systemic lupus erythematosus: hypomethylation of the IL10 and IL1R2 promoters is associated with disease activity. Genes Immun 13 (3): 214-220. Lin, W. C., Lin, C. F., Chen, C. L., Chen, C. W. and Lin, Y. S. (2010). Prediction of outcome in patients with acute respiratory distress syndrome by bronchoalveolar lavage inflammatory mediators. Exp Biol Med (Maywood) 235 (1): 57-65. Loercher, A. E., Nash, M. A., Kavanagh, J. J., Platsoucas, C. D. and Freedman, R. S. (1999). Identification of an IL-10-producing HLA-DR-negative monocyte subset in the malignant ascites of patients with ovarian carcinoma that inhibits cytokine protein expression and proliferation of autologous T cells. J Immunol 163 (11): 6251-6260. Longoni, D., Piemonti, L., Bernasconi, S., Mantovani, A. and Allavena, P. (1998). Interleukin-10 increases mannose receptor expression and endocytic activity in monocyte-derived dendritic cells. Int J Clin Lab Res 28 (3): 162-169. Lu, Y. C., Yeh, W. C. and Ohashi, P. S. (2008). LPS/TLR4 signal transduction pathway. Cytokine 42 (2): 145-151. Makdisi, G. and Wang, I. W. (2015). Extra Corporeal Membrane Oxygenation (ECMO) review of a lifesaving technology. J Thorac Dis 7 (7): E166-176. Malarstig, A., Eriksson, P., Hamsten, A., Lindahl, B., Wallentin, L. and Siegbahn, A. (2008). Raised interleukin-10 is an indicator of poor outcome and enhanced systemic inflammation in patients with acute coronary syndrome. Heart 94 (6): 724-729. Mann, D. L. (2011). The emerging role of innate immunity in the heart and vascular system: for whom the cell tolls. Circ Res 108 (9): 1133-1145. Mc, I. R. B., Timpa, J. G., Kurundkar, A. R., Holt, D. W., Kelly, D. R., Hartman, Y. E., et al. (2010). Plasma concentrations of inflammatory cytokines rise rapidly during ECMO-related SIRS due to the release of preformed stores in the intestine. Lab Invest 90 (1): 128-139. Millar, J. E., Fanning, J. P., McDonald, C. I., McAuley, D. F. and Fraser, J. F. (2016). The inflammatory response to extracorporeal membrane oxygenation (ECMO): a review of the pathophysiology. Crit Care 20 (1): 387. Monneret, G., Finck, M. E., Venet, F., Debard, A. L., Bohe, J., Bienvenu, J., et al. (2004). The anti-inflammatory response dominates after septic shock: association of low monocyte HLA-DR expression and high interleukin-10 concentration. Immunol Lett 95 (2): 193-198. Mullen, L., Hanschmann, E. M., Lillig, C. H., Herzenberg, L. A. and Ghezzi, P. (2015). Cysteine Oxidation Targets Peroxiredoxins 1 and 2 for Exosomal Release through a Novel Mechanism of Redox-Dependent Secretion. Mol Med 21 (1): 98-108. Palsson-McDermott, E. M. and O'Neill, L. A. (2004). Signal transduction by the lipopolysaccharide receptor, Toll-like receptor-4. Immunology 113 (2): 153-162. Pappalardo, F., Pieri, M., Greco, T., Patroniti, N., Pesenti, A., Arcadipane, A., et al. (2013). Predicting mortality risk in patients undergoing venovenous ECMO for ARDS due to influenza A (H1N1) pneumonia: the ECMOnet score. Intensive Care Med 39 (2): 275-281. Reuss, E., Fimmers, R., Kruger, A., Becker, C., Rittner, C. and Hohler, T. (2002). Differential regulation of interleukin-10 production by genetic and environmental factors--a twin study. Genes Immun 3 (7): 407-413. Reynolds, H. R. and Hochman, J. S. (2008). Cardiogenic shock: current concepts and improving outcomes. Circulation 117 (5): 686-697. Riddell, J. R., Wang, X. Y., Minderman, H. and Gollnick, S. O. (2010). Peroxiredoxin 1 stimulates secretion of proinflammatory cytokines by binding to TLR4. J Immunol 184 (2): 1022-1030. Roch, A., Hraiech, S., Masson, E., Grisoli, D., Forel, J. M., Boucekine, M., et al. (2014). Outcome of acute respiratory distress syndrome patients treated with extracorporeal membrane oxygenation and brought to a referral center. Intensive Care Med 40 (1): 74-83. Rubtsov, Y. P., Rasmussen, J. P., Chi, E. Y., Fontenot, J., Castelli, L., Ye, X., et al. (2008). Regulatory T cell-derived interleukin-10 limits inflammation at environmental interfaces. Immunity 28 (4): 546-558. Satoh, M., Shimoda, Y., Akatsu, T., Ishikawa, Y., Minami, Y. and Nakamura, M. (2006). Elevated circulating levels of heat shock protein 70 are related to systemic inflammatory reaction through monocyte Toll signal in patients with heart failure after acute myocardial infarction. Eur J Heart Fail 8 (8): 810-815. Satoh, M., Shimoda, Y., Maesawa, C., Akatsu, T., Ishikawa, Y., Minami, Y., et al. (2006). Activated toll-like receptor 4 in monocytes is associated with heart failure after acute myocardial infarction. Int J Cardiol 109 (2): 226-234. Schaaf, B., Luitjens, K., Goldmann, T., van Bremen, T., Sayk, F., Dodt, C., et al. (2009). Mortality in human sepsis is associated with downregulation of Toll-like receptor 2 and CD14 expression on blood monocytes. Diagn Pathol 4: 12. Schmidt, M., Bailey, M., Sheldrake, J., Hodgson, C., Aubron, C., Rycus, P. T., et al. (2014). Predicting survival after extracorporeal membrane oxygenation for severe acute respiratory failure. The Respiratory Extracorporeal Membrane Oxygenation Survival Prediction (RESP) score. Am J Respir Crit Care Med 189 (11): 1374-1382. Schmidt, M., Zogheib, E., Roze, H., Repesse, X., Lebreton, G., Luyt, C. E., et al. (2013). The PRESERVE mortality risk score and analysis of long-term outcomes after extracorporeal membrane oxygenation for severe acute respiratory distress syndrome. Intensive Care Med 39 (10): 1704-1713. Schneider, C. P., Schwacha, M. G. and Chaudry, I. H. (2004). The role of interleukin-10 in the regulation of the systemic inflammatory response following trauma-hemorrhage. Biochim Biophys Acta 1689 (1): 22-32. Shichita, T., Hasegawa, E., Kimura, A., Morita, R., Sakaguchi, R., Takada, I., et al. (2012). Peroxiredoxin family proteins are key initiators of post-ischemic inflammation in the brain. Nat Med 18 (6): 911-917. Shuto, T., Kato, K., Mori, Y., Viriyakosol, S., Oba, M., Furuta, T., et al. (2005). Membrane-anchored CD14 is required for LPS-induced TLR4 endocytosis in TLR4/MD-2/CD14 overexpressing CHO cells. Biochem Biophys Res Commun 338 (3): 1402-1409. Skrzeczynska-Moncznik, J., Bzowska, M., Loseke, S., Grage-Griebenow, E., Zembala, M. and Pryjma, J. (2008). Peripheral blood CD14high CD16+ monocytes are main producers of IL-10. Scand J Immunol 67 (2): 152-159. Sorensen, M. V., Pedersen, S., Mogelvang, R., Skov-Jensen, J. and Flyvbjerg, A. (2011). Plasma high-mobility group box 1 levels predict mortality after ST-segment elevation myocardial infarction. JACC Cardiovasc Interv 4 (3): 281-286. Thiagarajan, R. R., Barbaro, R. P., Rycus, P. T., McMullan, D. M., Conrad, S. A., Fortenberry, J. D., et al. (2017). Extracorporeal Life Support Organization Registry International Report 2016. Asaio J 63 (1): 60-67. Timmermans, K., Kox, M., Gerretsen, J., Peters, E., Scheffer, G. J., van der Hoeven, J. G., et al. (2015). The Involvement of Danger-Associated Molecular Patterns in the Development of Immunoparalysis in Cardiac Arrest Patients. Crit Care Med 43 (11): 2332-2338. Turner, D. M., Williams, D. M., Sankaran, D., Lazarus, M., Sinnott, P. J. and Hutchinson, I. V. (1997). An investigation of polymorphism in the interleukin-10 gene promoter. Eur J Immunogenet 24 (1): 1-8. Vieira, P. L., Christensen, J. R., Minaee, S., O'Neill, E. J., Barrat, F. J., Boonstra, A., et al. (2004). IL-10-secreting regulatory T cells do not express Foxp3 but have comparable regulatory function to naturally occurring CD4+CD25+ regulatory T cells. J Immunol 172 (10): 5986-5993. Waage, A., Brandtzaeg, P., Halstensen, A., Kierulf, P. and Espevik, T. (1989). The complex pattern of cytokines in serum from patients with meningococcal septic shock. Association between interleukin 6, interleukin 1, and fatal outcome. J Exp Med 169 (1): 333-338. Ward, N. S., Casserly, B. and Ayala, A. (2008). The compensatory anti-inflammatory response syndrome (CARS) in critically ill patients. Clin Chest Med 29 (4): 617-625, viii. Wilson, C. H., Zeile, S., Chataway, T., Nieuwenhuijs, V. B., Padbury, R. T. and Barritt, G. J. (2011). Increased expression of peroxiredoxin 1 and identification of a novel lipid-metabolizing enzyme in the early phase of liver ischemia reperfusion injury. Proteomics 11 (22): 4385-4396. Wood, Z. A., Schroder, E., Robin Harris, J. and Poole, L. B. (2003). Structure, mechanism and regulation of peroxiredoxins. Trends Biochem Sci 28 (1): 32-40. Wu, M. S., Wu, C. Y., Chen, C. J., Lin, M. T., Shun, C. T. and Lin, J. T. (2003). Interleukin-10 genotypes associate with the risk of gastric carcinoma in Taiwanese Chinese. Int J Cancer 104 (5): 617-623. Yanagisawa, R., Warabi, E., Inoue, K., Yanagawa, T., Koike, E., Ichinose, T., et al. (2012). Peroxiredoxin I null mice exhibits reduced acute lung inflammation following ozone exposure. J Biochem 152 (6): 595-601. Zanoni, I., Ostuni, R., Marek, L. R., Barresi, S., Barbalat, R., Barton, G. M., et al. (2011). CD14 controls the LPS-induced endocytosis of Toll-like receptor 4. Cell 147 (4): 868-880. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/67725 | - |
| dc.description.abstract | 葉克膜提供心肺衰竭有效的呼吸及循環系統支持，近幾年在心因性休克及急性呼吸窘迫症病人的使用大幅增加，然而，儘管新型儀器設備的改良及加護病房照護的改善，葉克膜病人總體死亡率仍居高不下。因此，了解造成不良預後的機制是改善病人選擇標準及精進介入治療方法的重要課題。
使用葉克膜可能引起缺血再灌流的傷害，與先天性免疫系統廣泛被激活有關，造成全身性發炎反應症狀，如果不受控制，將導致多重器官衰竭而死亡。本研究中，我們偵測血液中組織傷害所釋放之damage associated molecular pattern (DAMP) 分子第一型過氧化物還原酶Peroxiredoxin 1 (Prdx1)、發炎細胞激素、免疫細胞族群、及單核球表面先天性免疫受體 (TLR4 和CD14) 在病人裝置葉克膜前後的變化，來闡明全身性發炎反應的病因及找出可能的預後因子，以利葉克膜的妥善使用。 在心因性休克病人中，結果顯示葉克膜支持的早期，血液中Prdx1的濃度增加不僅比其他發炎激素更早達到高峰，而且血液中較高的Prdx1濃度可預測不良預後。Prdx1濃度和缺氧指標carbonic anhydrase IX 、乳酸及多項發炎激素濃度呈現正相關。人類單核球細胞的體外試驗也顯示，缺氧後再充氧會強化Prdx1所誘導的發炎激素產生，也使單核球細胞釋出Prdx1。進一步外加Prdx1抗體則可抑制此發炎激素 IL-6 的產生。這些結果說明葉克膜支持的早期，心因性休克病人血液中Prdx1的釋出可能和全身性發炎反應的形成及臨床不良預後有關。 急性呼吸窘迫症病人在裝置葉克膜前及隨後的六個小時，血液中高濃度的IL-10 是這些病人不良預後的潛力標誌物。這些在葉克膜支持初期所釋放出來的 IL-10濃度和重症加護病房常用的風險評估分數呈現正相關。高濃度IL-10可能涉及較慢的免疫細胞族群的比例恢復，如單核球細胞CD14+CD16+、CD14+TLR4+ 和調節性T細胞 T regulatory cells。從基因體變異的觀點，此高濃度IL-10和其基因啟動子區域的兩個多形性核苷酸 (–592C and –819C) 有關。 根據精準醫療的原則，我們的發現提供了心因性休克和急性呼吸窘迫症而裝置葉克膜病人所需要的治療預後和機制的訊息，將有助於未來發展新的治療策略。 | zh_TW |
| dc.description.abstract | Extracorporeal membrane oxygenation (ECMO) provides effective respiratory and circulatory support for cardiopulmonary arrest, and has been increasingly used for patients with cardiogenic shock and acute respiratory distress syndrome (ARDS) refractory to conventional therapies. However, the overall prognosis of these patients, despite significant advances in quality of the devices and in the management of intensive care unit, remains grave. Therefore, understanding the underlying mechanisms which contribute to poor clinical outcomes is a pivotal issue to improve patient selection as well as further refine this therapeutic intervention.
An ischemia/reperfusion injury testified during ECMO is systemic inflammatory response syndrome (SIRS) which is associated with the widespread activation of the innate immunity, which, if unconstrained, would result in multiple organ failure and eventual mortality. To understand the underlying mechanisms which contribute to SIRS and identify potential biomarker of predicting value for appropriate use of ECMO, plasma damage associated molecular pattern (DAMP) molecule peroxiredoxin 1 (Prdx1), inflammatory cytokines, immune cell populations, and signaling receptors of DAMP (TLR4 and CD14) were examined during the early and subsequent disease courses of adult patients who received ECMO support. In patients with cardiogenic shock, Prdx1 not only peaks earlier than all the other cytokines we study during the initial course of ECMO installation, but also predicts a worse outcome in patients who had higher initial Prdx1 plasma levels. The Prdx1 levels in patients positively correlate with hypoxic markers carbonic anhydrase IX and lactate, and inflammatory cytokines. An in vitro study demonstrates that hypoxia/re-oxygenation induced Prdx1 release from human monocytes and enhances the responsiveness of the monocytes in Prdx1-induced cytokine secretions. Furthermore, functional inhibition by Prdx1 antibody implicates a crucial role of Prdx1 in hypoxia/re-oxygenation-induced IL-6 secretion. These findings indicate that Prdx1 release during the early phase of ECMO support in cardiogenic shock patients is associated with the development of SIRS and poor clinical outcomes. For ARDS patients, high IL-10 level at the time of ECMO installation and during the first 6 hours after ECMO support stands as a promising biomarker associated with grave prognosis. The initial IL-10 level is correlated to other conventional risk evaluation scores as a predictive factor for survival, and furthermore, elevated IL-10 levels are also related to a delayed recovery of certain immune cell populations such as CD14+CD16+, CD14+TLR4+ monocytes, and T regulatory cells. Genetically, high interleukin-10 is associated to two polymorphic nucleotides (–592C and –819C) at the interleukin-10 gene promoter area. Our finding provides prognostic and mechanistic information on the outcomes of cardiogenic shock and severely respiratory distressed patients, and potentially paves the strategy to develop new therapeutic modality based on the principles of precision medicine. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-17T01:46:16Z (GMT). No. of bitstreams: 1 ntu-106-D02421002-1.pdf: 2789275 bytes, checksum: 0c578ad58734a7e3bdbac663d4021dd1 (MD5) Previous issue date: 2017 | en |
| dc.description.tableofcontents | Contents
Chapter 1: Introduction………………………………………………………………. 1 1.1. Current applications of ECMO……………………………………………….….… 1 1.2. The ischemia/reperfusion injury during ECMO…………..………….…….…....… 4 1.3. Relationship between SIRS and CARS……………………………...…..………… 5 1.4. Regulation of pro- and anti-inflammatory TLR4 signaling………..………..…..… 6 1.5. Relationship between Prdx1 and innate immune response……………………..….. 8 1.6. The role of DAMP and IL-10 in immunoparalysis ..………….………………… 10 1.7. The aim of the study…………………………………………………...…..….… 11 Chapter 2: Materials and Methods………………….….…………………….…….. 13 2.1. Study populations ………………………..………………………….…….…….. 13 2.2. Outcome definitions………………….....………..……………...…….….……... 14 2.2.1. Cardiogenic shock.……………..……………………………………..……. 14 2.2.2. ARDS.………………………………………………………………………. 14 2.3. Blood sampling…………………………..………...……………………..…….... 15 2.4. ROS determination.…………...…...………………………………………..…… 15 2.5. Flow cytometry……………...…………………………………….….…...……... 16 2.6. Plasma analysis………………...………………………………………………… 17 2.7. Cell culture treatment……………...…………………………………………….. 18 2.8. Hypoxic treatment……………...……………………….……………..………… 19 2.9. Cloning of human recombinant Prdx1 protein ………...………..………………. 19 2.10. Western blotting……………………………………..………...……..…….....… 20 2.11. Genotyping for genetic variants…………..……………..…………....……...… 21 2.12. Statistical analysis……………………………………..……………………… 21 Chapter 3: Results…………………………….…………………...………………. 23 3.1. Cardiogenic shock patients necessitating ECMO………………………………… 23 3.1.1. Demographics and clinical characteristics of the patients …………...……… 23 3.1.2. Prdx1 levels and hypoxia…………..…………………………………..…..… 23 3.1.3. Prdx1 and systemic inflammatory cytokines…………………..……….….… 24 3.1.4. TLR4 signaling activation………………………………………..….….…… 26 3.1.5. rPrdx1 induced cytokine secretions from IFN-γ priming macrophages….…. 26 3.1.6. Hypoxia enhanced rPrdx1-induced cytokine secretions from monocytes….... 27 3.1.7. Prdx1 stimulated IL-6 secretion under hypoxia/reoxygenation treatment…... 28 3.1.8. Prdx1 stimulation of cytokine secretion is structure-dependent………...….... 28 3.1.9. hrPrdx1 induces LPS tolerance……………....……………………...…..…… 29 3.2. ARDS patients receiving ECMO.………………………………………………… 29 3.2.1. Demographics and clinical characteristics of the patien…………………….. 29 3.2.2. Early elevation of IL-10 predicts clinical outcomes…………………...…..… 30 3.2.3. Tregs, CD14+CD16+, and CD14+TLR4+ cell populations were higher in survivors than non-survivors on day 3……….………..…………………….. 31 3.2.4. IL-10 level is an independent risk factor for ICU morta……………..…..….. 32 3.2.5. Predictive accuracies of IL-10 level compared to other risk scoring systems for ICU mortality for this study cohort………………………….…………… 33 3.2.6. IL-10 promotor variants are associated with the initial IL-10 levels and clinical outcomes……………………………………………………..……… 34 Chapter 4: Discussion and Perspectives..…………………………………...……… 36 Tables………………………………………….…………………..……...……..……. 48 Table 1. Demographic and clinical characteristics of the patients in this study according to their survival status at 7th day after receiving ECMO support…48 Table 2. Predictive values of Prdx1 and cytokines for 7-day all cause mortality rate…50 Table 3. Correlations between plasma Prdx1 and cytokines in cardiogenic shock patients at the indicated time points after receiving ECMO……...…..……… 51 Table 4. Comparison of baseline characteristics before implementation with ECMO of the study subjects according to their survival status at ICU discharge….... 52 Table 5. Univariate and multivariate logistic regression analyses for independent predictors of ICU mortality in the patients of this study…………….....……. 53 Table 6. Comparison of the predictive values of IL-10 levels and other risk-evaluation scores for ICU mortality in the study subjects…………………..…...……… 54 Table 7. Allele frequency and genotype distribution of the IL-10 promotor variants in the study subjects according to their status at the moment of ECMO removal……………………………………………..………...……………… 55 Table 8. Allele frequency and genotype distribution of the IL-10 promotor variants in the study subjects according to their plasma IL-10 levels at day 0………..… 56 Figures……………………………………………….……………………….………. 57 Figure 1. CD14 and TLR4 expressions on CD14+ monocytes analyzed by flow cytometry………………………………………………..………………...57 Figure 2. Prdx1 was an early phase predictor for the clinical outcomes of cardiogenic shock patients who received ECMO resuscitation………….. 58 Figure 3. ROS levels in the cardiogenic shock patients who received ECMO support………………………………………………….…….…………… 59 Figure 4. Correlation between Prdx1 and hypoxic markers……..………....………... 60 Figure 5. Comparison of inflammatory cytokine profiles between survivors and non-survivors who received ECMO support………………………..……. 61 Figure 6. ROC analysis for potential biomarkers in predicting outcome of patients with cardiogenic shock receiving ECMO support……………………...… 62 Figure 7. High initial Prdx1 1 level in cardiogenic shock patients who received ECMO support was associated with a poorer survival…………………… 63 Figure 8. High initial Prdx1 level in cardiogenic shock patients who received ECMO support was associated with a poorer event-free survival………... 64 Figure 9. Interaction of TLR4, CD14 and Prdx1 in cardiogenic shock patients who received ECMO support…………………………………….…….… 65 Figure 10. Prdx1 induces IL-6 and TNF-α production in INF-γ primed macrophage................................................................................................. 66 Figure 11. Hypoxia enhanced Prdx1 induced IL-6 and TNF-α production……..…….67 Figure 12. Prdx1 inhibition blocked hypoxia/re-oxygenation induced IL-6 secretion……...…………………………………………………………… 68 Figure 13. Cytokine inducing activity of Prdx1 was diminished by reducing agent DTT………………………...………………………………………………69 Figure 14. Release of Prdx1 from non-survivors of cardiogenic shock patients necessitating ECMO support…………………………………...……...… 70 Figure 15. Induction of LPS tolerance in human peripheral blood mononuclear cells by hrPrdx1……………………………………………….……...….. 71 Figure 16. Initial plasma IL-10 level was a better prognostic biomarker than IL- 6 and IL-8 in ARDS patients receiving ECMO support……………...…..… 72 Figure 17. Initial plasma IL-10 levels were associated with higher chances of organ failures and mortality in ARDS patients during ECMO support……...….. 74 Figure 18. Comparisons of immune cell profiles between survivors and non-survivors in ARDS patients who received ECMO support………..… 75 Figure 19. Comparisons of immune cell profiles between survivors and non-survivors in ARDS patients who received ECMO support…….……. 77 Figure 20. Comparisons of immune cell profiles according to initial IL-10 levels in ARDS patients receiving ECMO support………….……….…….……. 78 Figure 21. Kaplan–Meier analysis for 90-day survival probability in ARDS patients receiving ECMO support according to initial IL-10 levels and RESP scores…………………………………………………..…………............. 79 Figure 22. Effect of IL-10 genotypes on the initial plasma IL-10 concentrations and the 90-day survival probability after receiving ECMO support…..…. 80 References……………………..…………………….……………………….……….. 81 Appendix……………….……………….……………….……………………………. 92 博士班修業期間所發表之相關論文清冊 | |
| dc.language.iso | en | |
| dc.subject | 葉克膜 | zh_TW |
| dc.subject | 心因性休克 | zh_TW |
| dc.subject | 急性呼吸窘迫症 | zh_TW |
| dc.subject | 過氧化物還原? | zh_TW |
| dc.subject | 全身性發炎反應症候群 | zh_TW |
| dc.subject | 先天性免疫 | zh_TW |
| dc.subject | ECMO | en |
| dc.subject | cardiogenic shock | en |
| dc.subject | ARDS | en |
| dc.subject | Prdx1 | en |
| dc.subject | SIRS | en |
| dc.subject | innate immunity | en |
| dc.title | 免疫和發炎反應在臨床使用葉克膜之病人的預後意義 | zh_TW |
| dc.title | Prognostic significance of immune/inflammatory responses in patients receiving extracorporeal membrane oxygenation | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 105-2 | |
| dc.description.degree | 博士 | |
| dc.contributor.coadvisor | 陳益祥(Yih-Sharng Chen) | |
| dc.contributor.oralexamcommittee | 黃書健(Shu-Chien Huang),許秉寧(Ping-Ning Hsu),周財福(Tsai-Fwu Chou),林萍章(Pyng-Jing Lin) | |
| dc.subject.keyword | 葉克膜,心因性休克,急性呼吸窘迫症,過氧化物還原?,全身性發炎反應症候群,先天性免疫, | zh_TW |
| dc.subject.keyword | ECMO,cardiogenic shock,ARDS,Prdx1,SIRS,innate immunity, | en |
| dc.relation.page | 92 | |
| dc.identifier.doi | 10.6342/NTU201701238 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2017-07-27 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 臨床醫學研究所 | zh_TW |
| 顯示於系所單位： | 臨床醫學研究所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-106-1.pdf 未授權公開取用 | 2.72 MB | Adobe PDF |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。