Early and marked up-regulation of TNF-α in acute respiratory distress syndrome after cardiopulmonary bypass
Tao Li, Nanfu Luo, Lei Du, Jin Liu, Lina Gong, Jing Zhou
Early and marked up-regulation of TNF-α in acute respiratory distress syndrome after cardiopulmonary bypass
Despite the technique of cardiopulmonary bypass (CPB) improved the development of modern cardiac surgery, many factors during CPB have been reported to induce acute respiratory distress syndrome (ARDS). The present study was to investigate which pro-inflammatory factors involved in the early phase of ARDS. Ten patients underwent valve replacement surgery with or without ARDS were enrolled for analysis of pulmonary function and inflammatory factors release including white blood cell (WBC), neutrophils, CD11b, CD18, interleukin (IL)-8 and tumor necrosis factor-α (TNF-α). The results demonstrated that the ratio of arterial oxygen tension/fraction of inspire oxygen (PaO2/FiO2) was greatly reduced in ARDS patients, but only the release of TNF-α was significantly increased, which was reversely correlated to the values of PaO2/FiO2. Also, the count of neutrophils adhesive to pulmonary endothelial cells was significantly increased in ARDS patients. Therefore, we concluded that TNF-α was quickly up-regulated and involved in the pathogenesis of CPB-induced ARDS via guiding primed neutrophils to pulmonary interstitium.
tumor necrosis factor-α / cardiopulmonary bypass / inflammation / acute respiratory distress syndrome
[1] |
Wan S, LeClerc JL, Vincent JL. Inflammatory response to cardiopulmonary bypass: mechanisms involved and possible therapeutic strategies. Chest1997; 112(3): 676-692
CrossRef
Pubmed
Google scholar
|
[2] |
Matthay MA, Zimmerman GA, Esmon C, Bhattacharya J, Coller B, Doerschuk CM, Floros J, Gimbrone MA Jr, Hoffman E, Hubmayr RD, Leppert M, Matalon S, Munford R, Parsons P, Slutsky AS, Tracey KJ, Ward P, Gail DB, Harabin AL. Future research directions in acute lung injury: summary of a National Heart, Lung, and Blood Institute working group. Am J Respir Crit Care Med2003; 167(7): 1027-1035
CrossRef
Pubmed
Google scholar
|
[3] |
Spragg RG, Bernard GR, Checkley W, Curtis JR, Gajic O, Guyatt G, Hall J, Israel E, Jain M, Needham DM, Randolph AG, Rubenfeld GD, Schoenfeld D, Thompson BT, Ware LB, Young D, Harabin AL. Beyond mortality: future clinical research in acute lung injury. Am J Respir Crit Care Med2010; 181(10): 1121-1127
CrossRef
Pubmed
Google scholar
|
[4] |
Lin S, Walker J, Xu L, Gozal D, Yu J. Behaviours of pulmonary sensory receptors during development of acute lung injury in the rabbit. Exp Physiol2007; 92(4): 749-755
CrossRef
Pubmed
Google scholar
|
[5] |
Apostolakis E, Filos KS, Koletsis E, Dougenis D. Lung dysfunction following cardiopulmonary bypass. J Card Surg2010; 25(1): 47-55
CrossRef
Pubmed
Google scholar
|
[6] |
McGrath EE, Marriott HM, Lawrie A, Francis SE, Sabroe I, Renshaw SA, Dockrell DH, Whyte MKB. TNF-related apoptosis-inducing ligand (TRAIL) regulates inflammatory neutrophil apoptosis and enhances resolution of inflammation. J Leukoc Biol2011; 90(5): 855-865
CrossRef
Pubmed
Google scholar
|
[7] |
Strieter RM, Kunkel SL, Keane MP, Standiford TJ. Chemokines in lung injury: Thomas A. Neff Lecture. Chest1999; 116(1 Suppl): 103S-110S
CrossRef
Pubmed
Google scholar
|
[8] |
Wheeler AP, Bernard GR. Acute lung injury and the acute respiratory distress syndrome: a clinical review. Lancet2007; 369(9572): 1553-1564
CrossRef
Pubmed
Google scholar
|
[9] |
Matthay MA, Zimmerman GA. Acute lung injury and the acute respiratory distress syndrome: four decades of inquiry into pathogenesis and rational management. Am J Respir Cell Mol Biol2005; 33(4): 319-327
CrossRef
Pubmed
Google scholar
|
[10] |
Matthay MA, Zemans RL. The acute respiratory distress syndrome: pathogenesis and treatment. Annu Rev Pathol2011; 6(1): 147-163
CrossRef
Pubmed
Google scholar
|
[11] |
Cross LJ, Matthay MA. Biomarkers in acute lung injury: insights into the pathogenesis of acute lung injury. Crit Care Clin2011; 27(2): 355-377
CrossRef
Pubmed
Google scholar
|
[12] |
Bernard GR, Artigas A, Brigham KL, Carlet J, Falke K, Hudson L, Lamy M, Legall JR, Morris A, Spragg R. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med1994; 149(3 Pt 1): 818-824
Pubmed
|
[13] |
Ottonello L, Montecucco F, Bertolotto M, Arduino N, Mancini M, Corcione A, Pistoia V, Dallegri F. CCL3 (MIP-1α) induces in vitro migration of GM-CSF-primed human neutrophils via CCR5-dependent activation of ERK 1/2. Cell Signal2005; 17(3): 355-363
CrossRef
Pubmed
Google scholar
|
[14] |
Zemans RL, Colgan SP, Downey GP. Transepithelial migration of neutrophils: mechanisms and implications for acute lung injury. Am J Respir Cell Mol Biol2009; 40(5): 519-535
CrossRef
Pubmed
Google scholar
|
[15] |
Meyer-Hoffert U, Wiedow O. Neutrophil serine proteases: mediators of innate immune responses. Curr Opin Hematol2011; 18(1): 19-24
CrossRef
Pubmed
Google scholar
|
[16] |
May AE, Neumann FJ, Schömig A, Preissner KT. VLA-4 (α(4)β(1)) engagement defines a novel activation pathway for β(2) integrin-dependent leukocyte adhesion involving the urokinase receptor. Blood2000; 96(2): 506-513
Pubmed
|
[17] |
Lee WL, Downey GP. Neutrophil activation and acute lung injury. Curr Opin Crit Care2001; 7(1): 1-7
CrossRef
Pubmed
Google scholar
|
[18] |
Soehnlein O. Multiple roles for neutrophils in atherosclerosis. Circ Res2012; 110(6): 875-888
CrossRef
Pubmed
Google scholar
|
[19] |
Tandon R, Sha’afi RI, Thrall RS. Neutrophil β2-integrin upregulation is blocked by a p38 MAP kinase inhibitor. Biochem Biophys Res Commun2000; 270(3): 858-862
CrossRef
Pubmed
Google scholar
|
/
〈 | 〉 |