Metabolic consequences of sepsis-induced acute lung injury revealed by plasma ¹H-nuclear magnetic resonance quantitative metabolomics and computational analysis
Metabolomics is an emerging component of systems biology that may be a viable strategy for the identification and validation of physiologically relevant biomarkers. Nuclear magnetic resonance (NMR) spectroscopy allows for establishing quantitative data sets for multiple endogenous metabolites withou...
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Published in | American journal of physiology. Lung cellular and molecular physiology Vol. 300; no. 1; pp. L4 - L11 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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American Physiological Society
01.01.2011
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Abstract | Metabolomics is an emerging component of systems biology that may be a viable strategy for the identification and validation of physiologically relevant biomarkers. Nuclear magnetic resonance (NMR) spectroscopy allows for establishing quantitative data sets for multiple endogenous metabolites without preconception. Sepsis-induced acute lung injury (ALI) is a complex and serious illness associated with high morbidity and mortality for which there is presently no effective pharmacotherapy. The goal of this study was to apply ¹H-NMR based quantitative metabolomics with subsequent computational analysis to begin working towards elucidating the plasma metabolic changes associated with sepsis-induced ALI. To this end, this pilot study generated quantitative data sets that revealed differences between patients with ALI and healthy subjects in the level of the following metabolites: total glutathione, adenosine, phosphatidylserine, and sphingomyelin. Moreover, myoinositol levels were associated with acute physiology scores (APS) (ρ = -0.53, P = 0.05, q = 0.25) and ventilator-free days (ρ = -0.73, P = 0.005, q = 0.01). There was also an association between total glutathione and APS (ρ = 0.56, P = 0.04, q = 0.25). Computational network analysis revealed a distinct metabolic pathway for each metabolite. In summary, this pilot study demonstrated the feasibility of plasma ¹H-NMR quantitative metabolomics because it yielded a physiologically relevant metabolite data set that distinguished sepsis-induced ALI from health. In addition, it justifies the continued study of this approach to determine whether sepsis-induced ALI has a distinct metabolic phenotype and whether there are predictive biomarkers of severity and outcome in these patients. |
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AbstractList | Metabolomics is an emerging component of systems biology that may be a viable strategy for the identification and validation of physiologically relevant biomarkers. Nuclear magnetic resonance (NMR) spectroscopy allows for establishing quantitative data sets for multiple endogenous metabolites without preconception. Sepsis-induced acute lung injury (ALI) is a complex and serious illness associated with high morbidity and mortality for which there is presently no effective pharmacotherapy. The goal of this study was to apply ¹H-NMR based quantitative metabolomics with subsequent computational analysis to begin working towards elucidating the plasma metabolic changes associated with sepsis-induced ALI. To this end, this pilot study generated quantitative data sets that revealed differences between patients with ALI and healthy subjects in the level of the following metabolites: total glutathione, adenosine, phosphatidylserine, and sphingomyelin. Moreover, myoinositol levels were associated with acute physiology scores (APS) (ρ = -0.53, P = 0.05, q = 0.25) and ventilator-free days (ρ = -0.73, P = 0.005, q = 0.01). There was also an association between total glutathione and APS (ρ = 0.56, P = 0.04, q = 0.25). Computational network analysis revealed a distinct metabolic pathway for each metabolite. In summary, this pilot study demonstrated the feasibility of plasma ¹H-NMR quantitative metabolomics because it yielded a physiologically relevant metabolite data set that distinguished sepsis-induced ALI from health. In addition, it justifies the continued study of this approach to determine whether sepsis-induced ALI has a distinct metabolic phenotype and whether there are predictive biomarkers of severity and outcome in these patients.Metabolomics is an emerging component of systems biology that may be a viable strategy for the identification and validation of physiologically relevant biomarkers. Nuclear magnetic resonance (NMR) spectroscopy allows for establishing quantitative data sets for multiple endogenous metabolites without preconception. Sepsis-induced acute lung injury (ALI) is a complex and serious illness associated with high morbidity and mortality for which there is presently no effective pharmacotherapy. The goal of this study was to apply ¹H-NMR based quantitative metabolomics with subsequent computational analysis to begin working towards elucidating the plasma metabolic changes associated with sepsis-induced ALI. To this end, this pilot study generated quantitative data sets that revealed differences between patients with ALI and healthy subjects in the level of the following metabolites: total glutathione, adenosine, phosphatidylserine, and sphingomyelin. Moreover, myoinositol levels were associated with acute physiology scores (APS) (ρ = -0.53, P = 0.05, q = 0.25) and ventilator-free days (ρ = -0.73, P = 0.005, q = 0.01). There was also an association between total glutathione and APS (ρ = 0.56, P = 0.04, q = 0.25). Computational network analysis revealed a distinct metabolic pathway for each metabolite. In summary, this pilot study demonstrated the feasibility of plasma ¹H-NMR quantitative metabolomics because it yielded a physiologically relevant metabolite data set that distinguished sepsis-induced ALI from health. In addition, it justifies the continued study of this approach to determine whether sepsis-induced ALI has a distinct metabolic phenotype and whether there are predictive biomarkers of severity and outcome in these patients. Metabolomics is an emerging component of systems biology that may be a viable strategy for the identification and validation of physiologically relevant biomarkers. Nuclear magnetic resonance (NMR) spectroscopy allows for establishing quantitative data sets for multiple endogenous metabolites without preconception. Sepsis-induced acute lung injury (ALI) is a complex and serious illness associated with high morbidity and mortality for which there is presently no effective pharmacotherapy. The goal of this study was to apply 1 H-NMR based quantitative metabolomics with subsequent computational analysis to begin working towards elucidating the plasma metabolic changes associated with sepsis-induced ALI. To this end, this pilot study generated quantitative data sets that revealed differences between patients with ALI and healthy subjects in the level of the following metabolites: total glutathione, adenosine, phosphatidylserine, and sphingomyelin. Moreover, myoinositol levels were associated with acute physiology scores (APS) (ρ = −0.53, P = 0.05, q = 0.25) and ventilator-free days (ρ = −0.73, P = 0.005, q = 0.01). There was also an association between total glutathione and APS (ρ = 0.56, P = 0.04, q = 0.25). Computational network analysis revealed a distinct metabolic pathway for each metabolite. In summary, this pilot study demonstrated the feasibility of plasma 1 H-NMR quantitative metabolomics because it yielded a physiologically relevant metabolite data set that distinguished sepsis-induced ALI from health. In addition, it justifies the continued study of this approach to determine whether sepsis-induced ALI has a distinct metabolic phenotype and whether there are predictive biomarkers of severity and outcome in these patients. Metabolomics is an emerging component of systems biology that may be a viable strategy for the identification and validation of physiologically relevant biomarkers. Nuclear magnetic resonance (NMR) spectroscopy allows for establishing quantitative data sets for multiple endogenous metabolites without preconception. Sepsis-induced acute lung injury (ALI) is a complex and serious illness associated with high morbidity and mortality for which there is presently no effective pharmacotherapy. The goal of this study was to apply ¹H-NMR based quantitative metabolomics with subsequent computational analysis to begin working towards elucidating the plasma metabolic changes associated with sepsis-induced ALI. To this end, this pilot study generated quantitative data sets that revealed differences between patients with ALI and healthy subjects in the level of the following metabolites: total glutathione, adenosine, phosphatidylserine, and sphingomyelin. Moreover, myoinositol levels were associated with acute physiology scores (APS) (ρ = -0.53, P = 0.05, q = 0.25) and ventilator-free days (ρ = -0.73, P = 0.005, q = 0.01). There was also an association between total glutathione and APS (ρ = 0.56, P = 0.04, q = 0.25). Computational network analysis revealed a distinct metabolic pathway for each metabolite. In summary, this pilot study demonstrated the feasibility of plasma ¹H-NMR quantitative metabolomics because it yielded a physiologically relevant metabolite data set that distinguished sepsis-induced ALI from health. In addition, it justifies the continued study of this approach to determine whether sepsis-induced ALI has a distinct metabolic phenotype and whether there are predictive biomarkers of severity and outcome in these patients. Metabolomics is an emerging component of systems biology that may be a viable strategy for the identification and validation of physiologically relevant biomarkers. Nuclear magnetic resonance (NMR) spectroscopy allows for establishing quantitative data sets for multiple endogenous metabolites without preconception. Sepsis-induced acute lung injury (ALI) is a complex and serious illness associated with high morbidity and mortality for which there is presently no effective pharmacotherapy. The goal of this study was to apply 1H-NMR based quantitative metabolomics with subsequent computational analysis to begin working towards elucidating the plasma metabolic changes associated with sepsis-induced ALI. To this end, this pilot study generated quantitative data sets that revealed differences between patients with ALI and healthy subjects in the level of the following metabolites: total glutathione, adenosine, phosphatidylserine, and sphingomyelin. Moreover, myoinositol levels were associated with acute physiology scores (APS) ( rho = -0.53, P = 0.05, q = 0.25) and ventilator-free days ( rho = -0.73, P = 0.005, q = 0.01). There was also an association between total glutathione and APS ( rho = 0.56, P = 0.04, q = 0.25). Computational network analysis revealed a distinct metabolic pathway for each metabolite. In summary, this pilot study demonstrated the feasibility of plasma 1H-NMR quantitative metabolomics because it yielded a physiologically relevant metabolite data set that distinguished sepsis-induced ALI from health. In addition, it justifies the continued study of this approach to determine whether sepsis-induced ALI has a distinct metabolic phenotype and whether there are predictive biomarkers of severity and outcome in these patients. |
Author | Serkova, Natalie J Paine, 3rd, Robert Karnovsky, Alla Standiford, Theodore J Stringer, Kathleen A Guire, Kenneth |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 K. A. Stringer and N. J. Serkova contributed equally to this work. |
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References | 20139469 - Bioinformatics. 2010 Apr 1;26(7):971-3 16680201 - Metabolomics. 2005 Mar;1(1):3-9 18179359 - Antioxid Redox Signal. 2008 Apr;10(4):739-53 20228181 - Am J Physiol Lung Cell Mol Physiol. 2010 Jun;298(6):L755-67 8989170 - Crit Care Med. 1997 Jan;25(1):9-15 15698456 - Kidney Int. 2005 Mar;67(3):1142-51 7316475 - Ann Hum Genet. 1981 Feb;45(Pt 1):15-9 18658106 - Am J Respir Crit Care Med. 2008 Oct 1;178(7):701-9 19428331 - Biochem Pharmacol. 2009 Jun 15;77(12):1763-72 19480633 - Biotechniques. 2009 Apr;46(5):363-5 16909368 - Semin Respir Crit Care Med. 2006 Aug;27(4):337-49 12120097 - Nat Rev Drug Discov. 2002 Feb;1(2):153-61 15627238 - NMR Biomed. 2005 May;18(3):143-62 11706287 - Curr Opin Clin Nutr Metab Care. 2001 Nov;4(6):521-6 9700100 - Am J Physiol. 1998 Aug;275(2 Pt 1):L379-88 11706283 - Curr Opin Clin Nutr Metab Care. 2001 Nov;4(6):499-502 12091165 - Am J Respir Crit Care Med. 2002 Jul 1;166(1):16-20 18403332 - Proc Am Thorac Soc. 2008 Apr 15;5(3):348-53 18755926 - Am J Respir Crit Care Med. 2008 Dec 1;178(11):1100-14 7509706 - Am J Respir Crit Care Med. 1994 Mar;149(3 Pt 1):818-24 18953024 - Nucleic Acids Res. 2009 Jan;37(Database issue):D603-10 18760298 - Mol Aspects Med. 2009 Feb-Apr;30(1-2):60-76 18171018 - Chem Res Toxicol. 2008 Jan;21(1):9-27 19835422 - J Proteome Res. 2009 Dec;8(12):5423-30 18441091 - Am J Physiol Lung Cell Mol Physiol. 2008 Jul;295(1):L152-61 19201926 - Am J Respir Crit Care Med. 2009 May 1;179(9):806-15 19948758 - Nucleic Acids Res. 2010 Jan;38(Database issue):D480-7 15789454 - Am J Physiol Regul Integr Comp Physiol. 2004 Aug;287(2):R247-9 17016518 - Mol Syst Biol. 2006;2:52 19864339 - Am J Physiol Regul Integr Comp Physiol. 2010 Jan;298(1):R166-72 17900487 - Crit Care Clin. 2007 Jul;23(3):639-58 12324551 - N Engl J Med. 2002 Sep 26;347(13):966-7 17882155 - Mol Syst Biol. 2007;3:135 16222040 - Proc Am Thorac Soc. 2005;2(3):214-20 12133657 - Lancet. 2002 Jul 20;360(9328):219-23 17202168 - Nucleic Acids Res. 2007 Jan;35(Database issue):D521-6 20479934 - PLoS One. 2010;5(5):e10538 20457745 - Nucleic Acids Res. 2010 Jul;38(Web Server issue):W71-7 17396131 - Cell Death Differ. 2007 Jul;14(7):1315-23 18020967 - Clin Chem Lab Med. 2008;46(1):27-42 17009906 - Expert Rev Mol Diagn. 2006 Sep;6(5):717-31 17360481 - Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4083-8 18203816 - Am J Physiol Lung Cell Mol Physiol. 2008 Apr;294(4):L632-41 19494329 - J Immunol. 2009 Jun 15;182(12):8037-46 |
References_xml | – reference: 18658106 - Am J Respir Crit Care Med. 2008 Oct 1;178(7):701-9 – reference: 19480633 - Biotechniques. 2009 Apr;46(5):363-5 – reference: 17016518 - Mol Syst Biol. 2006;2:52 – reference: 18171018 - Chem Res Toxicol. 2008 Jan;21(1):9-27 – reference: 16680201 - Metabolomics. 2005 Mar;1(1):3-9 – reference: 19201926 - Am J Respir Crit Care Med. 2009 May 1;179(9):806-15 – reference: 20139469 - Bioinformatics. 2010 Apr 1;26(7):971-3 – reference: 15789454 - Am J Physiol Regul Integr Comp Physiol. 2004 Aug;287(2):R247-9 – reference: 17009906 - Expert Rev Mol Diagn. 2006 Sep;6(5):717-31 – reference: 18953024 - Nucleic Acids Res. 2009 Jan;37(Database issue):D603-10 – reference: 8989170 - Crit Care Med. 1997 Jan;25(1):9-15 – reference: 11706287 - Curr Opin Clin Nutr Metab Care. 2001 Nov;4(6):521-6 – reference: 11706283 - Curr Opin Clin Nutr Metab Care. 2001 Nov;4(6):499-502 – reference: 19948758 - Nucleic Acids Res. 2010 Jan;38(Database issue):D480-7 – reference: 19494329 - J Immunol. 2009 Jun 15;182(12):8037-46 – reference: 18441091 - Am J Physiol Lung Cell Mol Physiol. 2008 Jul;295(1):L152-61 – reference: 7509706 - Am J Respir Crit Care Med. 1994 Mar;149(3 Pt 1):818-24 – reference: 20228181 - Am J Physiol Lung Cell Mol Physiol. 2010 Jun;298(6):L755-67 – reference: 17202168 - Nucleic Acids Res. 2007 Jan;35(Database issue):D521-6 – reference: 17360481 - Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4083-8 – reference: 18179359 - Antioxid Redox Signal. 2008 Apr;10(4):739-53 – reference: 18403332 - Proc Am Thorac Soc. 2008 Apr 15;5(3):348-53 – reference: 9700100 - Am J Physiol. 1998 Aug;275(2 Pt 1):L379-88 – reference: 18755926 - Am J Respir Crit Care Med. 2008 Dec 1;178(11):1100-14 – reference: 17396131 - Cell Death Differ. 2007 Jul;14(7):1315-23 – reference: 19835422 - J Proteome Res. 2009 Dec;8(12):5423-30 – reference: 12133657 - Lancet. 2002 Jul 20;360(9328):219-23 – reference: 20457745 - Nucleic Acids Res. 2010 Jul;38(Web Server issue):W71-7 – reference: 17900487 - Crit Care Clin. 2007 Jul;23(3):639-58 – reference: 15698456 - Kidney Int. 2005 Mar;67(3):1142-51 – reference: 7316475 - Ann Hum Genet. 1981 Feb;45(Pt 1):15-9 – reference: 16909368 - Semin Respir Crit Care Med. 2006 Aug;27(4):337-49 – reference: 19864339 - Am J Physiol Regul Integr Comp Physiol. 2010 Jan;298(1):R166-72 – reference: 12091165 - Am J Respir Crit Care Med. 2002 Jul 1;166(1):16-20 – reference: 12324551 - N Engl J Med. 2002 Sep 26;347(13):966-7 – reference: 17882155 - Mol Syst Biol. 2007;3:135 – reference: 19428331 - Biochem Pharmacol. 2009 Jun 15;77(12):1763-72 – reference: 15627238 - NMR Biomed. 2005 May;18(3):143-62 – reference: 18203816 - Am J Physiol Lung Cell Mol Physiol. 2008 Apr;294(4):L632-41 – reference: 18760298 - Mol Aspects Med. 2009 Feb-Apr;30(1-2):60-76 – reference: 12120097 - Nat Rev Drug Discov. 2002 Feb;1(2):153-61 – reference: 20479934 - PLoS One. 2010;5(5):e10538 – reference: 16222040 - Proc Am Thorac Soc. 2005;2(3):214-20 – reference: 18020967 - Clin Chem Lab Med. 2008;46(1):27-42 |
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SubjectTerms | Acute Lung Injury - blood Acute Lung Injury - pathology Humans Magnetic Resonance Spectroscopy - methods Metabolomics - methods Metabolomics - trends Phenotype Pilot Projects Reference Values Sepsis - blood Sepsis - complications Sepsis - genetics |
Title | Metabolic consequences of sepsis-induced acute lung injury revealed by plasma ¹H-nuclear magnetic resonance quantitative metabolomics and computational analysis |
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