Suspension microarrays for the identification of the response patterns in hyperinflammatory diseases.

Miniaturized and parallelized sandwich immunoassays allow the simultaneous analysis of a variety of parameters in a single experiment. Bead-based protein array systems or suspension microarrays are well-established multiplex sandwich immunoassay formats. To study inflammatory diseases, protein arrays can be used to analyze changes in plasma protein levels, such as cytokines, chemokines, soluble receptors, and matrix metalloproteinases. Using the bead-based Luminex system, multiplexed sandwich immunoassays have been developed to analyze the plasma concentrations of soluble receptors: sTNF-RI, sTNF-RII, sIL-2R, sgp130, sFas, sRAGE, sE-selectin, sICAM-1, sVCAM-1, sMIF-1 and sFasL. This newly established 11-plex soluble receptors assay demonstrated acceptable intra-assay and inter-assay precision, appropriate accuracy, and no crossreactivity between analytes. Using this assay, 100 plasma samples derived from 36 critically ill intensive care unit (ICU) patients with trauma or sepsis were analyzed for their soluble receptor plasma concentrations. Results obtained allowed grouping of patients' samples into a trauma and a sepsis group. Four candidate molecules: sFas, sICAM-1, sTNF-RI, and sTNF-RII had higher concentrations in patients with sepsis than in those with trauma, contributing the highest discriminatory values to define the nature of the inflammatory disease originating from pathogen-involved (sepsis) or pathogen-independent inflammation.

[1]  R. Hotchkiss,et al.  Apoptosis and caspases regulate death and inflammation in sepsis , 2006, Nature Reviews Immunology.

[2]  Dieter Stoll,et al.  Protein microarrays and multiplexed sandwich immunoassays: what beats the beads? , 2004, Combinatorial chemistry & high throughput screening.

[3]  W. Knaus,et al.  Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. 1992. , 2009, Chest.

[4]  R. Korthuis,et al.  Role of neutrophil-endothelial cell adhesion in inflammatory disorders. , 1994, Journal of critical care.

[5]  W. Knaus,et al.  Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. , 1992, Chest.

[6]  S. Kingsmore.  Multiplexed protein measurement: technologies and applications of protein and antibody arrays , 2006, Nature Reviews Drug Discovery.

[7]  T. Joos,et al.  Caspase‐3 Activation, Bcl‐2 Contents, and Soluble FAS‐Ligand Are Not Related to the Inflammatory Marker Profile in Patients with Sepsis and Septic Shock , 2006, Annals of the New York Academy of Sciences.

[8]  R. Hotchkiss,et al.  Rapid onset of intestinal epithelial and lymphocyte apoptotic cell death in patients with trauma and shock , 2000, Critical care medicine.

[9]  T. Scalea,et al.  Persistent systemic inflammatory response syndrome is predictive of nosocomial infection in trauma. , 2002, The Journal of trauma.

[10]  L. Moldawer,et al.  Correlation between acute physiology and chronic health evaluation (APACHE) III score and immunological parameters in critically ill patients with sepsis , 1996, The British journal of surgery.

[11]  N. Vaziri,et al.  Soluble cytokine receptors and receptor antagonists are sequentially released after trauma. , 1995, The Journal of trauma.

[12]  Dieter Stoll,et al.  Protein microarrays: applications and future challenges. , 2005, Current opinion in drug discovery & development.

[13]  U. Prabhakar,et al.  Simultaneous quantification of proinflammatory cytokines in human plasma using the LabMAP assay. , 2002, Journal of immunological methods.

[14]  Peter A. Ward,et al.  Novel strategies for the treatment of sepsis , 2003, Nature Medicine.

[15]  J. Vincent,et al.  Serum cytokine levels in human septic shock. Relation to multiple-system organ failure and mortality. , 1993, Chest.

[16]  L. Moldawer,et al.  SEPSIS SYNDROMES: UNDERSTANDING THE ROLE OF INNATE AND ACQUIRED IMMUNITY , 2001, Shock.

[17]  Corinne Alberti,et al.  Epidemiology of sepsis and infection in ICU patients from an international multicentre cohort study , 2002, Intensive Care Medicine.

[18]  R. L. Grubbs,et al.  Evaluation of protein C and other biomarkers as predictors of mortality in a rat cecal ligation and puncture model of sepsis* , 2004, Critical care medicine.

[19]  A I Saeed,et al.  TM4: a free, open-source system for microarray data management and analysis. , 2003, BioTechniques.

[20]  Margaret M Parker,et al.  Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock , 2004, Critical care medicine.

[21]  J. Jais,et al.  Elevated circulating E-selectin, intercellular adhesion molecule 1, and von Willebrand factor in patients with severe infection. , 1998, American journal of respiratory and critical care medicine.

[22]  M. Cuesta,et al.  Increased soluble interleukin-1 type II receptor concentrations in postoperative patients and in patients with sepsis syndrome. , 1996, Blood.

[23]  Jingyong Zhao,et al.  Adoptive Transfer of In Vitro-Stimulated CD4+CD25+ Regulatory T Cells Increases Bacterial Clearance and Improves Survival in Polymicrobial Sepsis , 2005, The Journal of Immunology.

[24]  L. Moldawer,et al.  Interleukin-1 receptor antagonist circulates in experimental inflammation and in human disease. , 1992, Blood.

[25]  J. Mege,et al.  Systemic endothelial activation is greater in septic than in traumatic-hemorrhagic shock but does not correlate with endothelial activation in skin biopsies , 2002, Critical care medicine.

[26]  N. Hogg.  Roll, roll, roll your leucocyte gently down the vein.... , 1992, Immunology today.

[27]  F. Ramsdell,et al.  Fas and FasL in the homeostatic regulation of immune responses. , 1995, Immunology today.

[28]  R. Cotran,et al.  Leukocytosis and resistance to septic shock in intercellular adhesion molecule 1-deficient mice , 1994, The Journal of experimental medicine.

[29]  P. Matzinger.  The Danger Model: A Renewed Sense of Self , 2002, Science.

[30]  D. Cummins,et al.  Multiplex proteomic approaches to sepsis research: case studies employing new technologies , 2005, Expert review of proteomics.

[31]  A. Agadir,et al.  Cytometric bead array: a multiplexed assay platform with applications in various areas of biology. , 2004, Clinical immunology.

[32]  M. Scott,et al.  TWEAK Is a Novel Arthritogenic Mediator , 2006, The Journal of Immunology.

[33]  T. Yokota,et al.  Expression of the Fas ligand in cells of T cell lineage. , 1995, Journal of immunology.

[34]  Joshua R. Ehrlich,et al.  Autoantibody microarrays for biomarker discovery , 2007, Expert review of proteomics.

[35]  R. Bone,et al.  Sir Isaac Newton, sepsis, SIRS, and CARS. , 1996, Critical care medicine.

[36]  J. Cardier,et al.  Serum levels of the apoptosis-associated molecules, tumor necrosis factor-alpha/tumor necrosis factor type-I receptor and Fas/FasL, in sepsis. , 2004, Chest.

[37]  H. Redmond,et al.  Cellular Apoptosis and Organ Injury in Sepsis: A Review , 2002, Shock.

[38]  J. W. Findlay,et al.  Validation of immunoassays for bioanalysis: a pharmaceutical industry perspective. , 2000, Journal of pharmaceutical and biomedical analysis.

[39]  I. Yaniv,et al.  Induction of tolerance using Fas ligand: a double-edged immunomodulator. , 2005, Blood.

[40]  George Scott,et al.  Toward resolving the challenges of sepsis diagnosis. , 2004, Clinical chemistry.

[41]  Marta Sanchez-Carbayo,et al.  Antibody arrays: technical considerations and clinical applications in cancer. , 2006, Clinical chemistry.

[42]  W. Kuis,et al.  Peripheral Blood Mononuclear Cells Cytokines in a Single Sample of Stimulated Simultaneous Detection of 15 Human , 2002 .

[43]  Mitchell M. Levy,et al.  Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock , 2004, Critical care medicine.

[44]  C. Sessler,et al.  Circulating ICAM-1 is increased in septic shock. , 1995, American journal of respiratory and critical care medicine.

[45]  P. Barie,et al.  Monocyte tumor necrosis factor receptor levels as a predictor of risk in human sepsis. , 1996, Archives of surgery.

[46]  H. Horvitz,et al.  MicroRNA expression profiles classify human cancers , 2005, Nature.

[47]  H. Volk,et al.  Immunologic and hemodynamic effects of "low-dose" hydrocortisone in septic shock: a double-blind, randomized, placebo-controlled, crossover study. , 2003, American journal of respiratory and critical care medicine.

[48]  J. Marshall,et al.  Clinical trials of mediator-directed therapy in sepsis: what have we learned? , 2000, Intensive Care Medicine.

[49]  D. Mannino,et al.  The epidemiology of sepsis in the United States from 1979 through 2000. , 2003, The New England journal of medicine.

[50]  R. Mage,et al.  A comparison of ELISA and flow microsphere-based assays for quantification of immunoglobulins. , 2002, Journal of immunological methods.

[51]  R. Strieter,et al.  Acute lung injury: the role of cytokines in the elicitation of neutrophils. , 1994, Journal of investigative medicine : the official publication of the American Federation for Clinical Research.

[52]  C. Ballantyne,et al.  Multiplexed analysis of biomarkers related to obesity and the metabolic syndrome in human plasma, using the Luminex-100 system. , 2005, Clinical chemistry.