This information is current as Inflammasome in Lung Endothelial Cells Hemorrhagic Shock Activation of NLRP 3
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M. Wilson | T. Billiar | L. Yin | Jie Fan | G. Xiao | M. Scott | Yuehua Li | M. Xiang | Jia Xu | Xiaoli Shi
[1] Y. Vodovotz,et al. Hemorrhagic shock activates lung endothelial reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase via neutrophil NADPH oxidase. , 2011, American journal of respiratory cell and molecular biology.
[2] M. Lamkanfi. Emerging inflammasome effector mechanisms , 2011, Nature Reviews Immunology.
[3] E. Mazzon,et al. Effect of apocynin, a NADPH oxidase inhibitor, on acute lung inflammation. , 2011, Biochemical pharmacology.
[4] J. Tschopp,et al. NLRP3 inflammasome activation: the convergence of multiple signalling pathways on ROS production? , 2010, Nature Reviews Immunology.
[5] J. Tschopp,et al. Thioredoxin-interacting protein links oxidative stress to inflammasome activation , 2010, Nature Immunology.
[6] Y. Vodovotz,et al. Hemorrhagic shock augments lung endothelial cell activation: role of temporal alterations of TLR4 and TLR2. , 2009, American journal of physiology. Regulatory, integrative and comparative physiology.
[7] A. Sauaia,et al. HMGB1 IS MARKEDLY ELEVATED WITHIN 6 HOURS OF MECHANICAL TRAUMA IN HUMANS , 2009, Shock.
[8] Y. Vodovotz,et al. Interacting Neuroendocrine and Innate and Acquired Immune Pathways Regulate Neutrophil Mobilization from Bone Marrow following Hemorrhagic Shock1 , 2009, The Journal of Immunology.
[9] J. Tschopp,et al. Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica , 2008, Science.
[10] T. Billiar,et al. Early events in the recognition of danger signals after tissue injury , 2008, Journal of leukocyte biology.
[11] F. Martinon,et al. Activation of the NALP3 inflammasome is triggered by low intracellular potassium concentration , 2007, Cell Death and Differentiation.
[12] K. Tracey,et al. Hemorrhagic Shock Induces NAD(P)H Oxidase Activation in Neutrophils: Role of HMGB1-TLR4 Signaling1 , 2007, The Journal of Immunology.
[13] E. Chavakis,et al. A novel pathway of HMGB1‐mediated inflammatory cell recruitment that requires Mac‐1‐integrin , 2007, The EMBO journal.
[14] Y. Vodovotz,et al. Hemorrhagic shock-activated neutrophils augment TLR4 signaling-induced TLR2 upregulation in alveolar macrophages: role in hemorrhage-primed lung inflammation. , 2006, American journal of physiology. Lung cellular and molecular physiology.
[15] E. Abraham,et al. High mobility group box 1 protein interacts with multiple Toll-like receptors. , 2006, American journal of physiology. Cell physiology.
[16] M. Lotze,et al. Hepatic Ischemia/Reperfusion Injury Involves Functional TLR4 Signaling in Nonparenchymal Cells1 , 2005, The Journal of Immunology.
[17] I. Douglas,et al. HMGB1 contributes to the development of acute lung injury after hemorrhage. , 2005, American journal of physiology. Lung cellular and molecular physiology.
[18] K. Tracey,et al. The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion , 2005, The Journal of experimental medicine.
[19] M. Lotze,et al. Addicted to Death: Invasive Cancer and the Immune Response to Unscheduled Cell Death , 2005, Journal of immunotherapy.
[20] C. Roussos,et al. Pulmonary endothelium in acute lung injury: from basic science to the critically ill , 2004, Intensive Care Medicine.
[21] U. Andersson,et al. Mini‐review: The nuclear protein HMGB1 as a proinflammatory mediator , 2004, European journal of immunology.
[22] E. Abraham,et al. Involvement of Toll-like Receptors 2 and 4 in Cellular Activation by High Mobility Group Box 1 Protein* , 2004, Journal of Biological Chemistry.
[23] K. Tracey,et al. Reversing established sepsis with antagonists of endogenous high-mobility group box 1 , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[24] R. Frey,et al. TLR4 signaling induces TLR2 expression in endothelial cells via neutrophil NADPH oxidase. , 2003, The Journal of clinical investigation.
[25] A. Ridley,et al. Receptor for advanced glycation end products-binding COOH-terminal motif of amphoterin inhibits invasive migration and metastasis. , 2002, Cancer research.
[26] F. Martinon,et al. The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta. , 2002, Molecular cell.
[27] M. Freichel,et al. Impairment of Store-Operated Ca2+ Entry in TRPC4−/− Mice Interferes With Increase in Lung Microvascular Permeability , 2002, Circulation research.
[28] P. Matzinger. The Danger Model: A Renewed Sense of Self , 2002, Science.
[29] K. Tracey,et al. HMGB1 as a late mediator of lethal systemic inflammation. , 2001, American journal of respiratory and critical care medicine.
[30] M. J. Cotter,et al. A novel method for isolation of neutrophils from murine blood using negative immunomagnetic separation. , 2001, The American journal of pathology.
[31] B. Babior. The NADPH Oxidase of Endothelial Cells , 2000, IUBMB life.
[32] K. Tracey,et al. High Mobility Group 1 Protein (Hmg-1) Stimulates Proinflammatory Cytokine Synthesis in Human Monocytes , 2000, The Journal of experimental medicine.
[33] L. Moldawer,et al. ANTICYTOKINE THERAPIES FOR ACUTE INFLAMMATION AND THE SYSTEMIC INFLAMMATORY RESPONSE SYNDROME: IL‐10 AND ISCHEMIA/REPERFUSION INJURY AS A NEW PARADIGM , 2000, Shock.
[34] D. Sorescu,et al. NAD(P)H oxidase: role in cardiovascular biology and disease. , 2000, Circulation research.
[35] K. Tracey,et al. HMG-1 as a late mediator of endotoxin lethality in mice. , 1999, Science.
[36] H. Huttunen,et al. Receptor for Advanced Glycation End Products (RAGE)-mediated Neurite Outgrowth and Activation of NF-κB Require the Cytoplasmic Domain of the Receptor but Different Downstream Signaling Pathways* , 1999, The Journal of Biological Chemistry.
[37] E. Abraham,et al. Why immunomodulatory therapies have not worked in sepsis , 1999, Intensive Care Medicine.
[38] A. Al-Mehdi,et al. Endothelial NADPH oxidase as the source of oxidants in lungs exposed to ischemia or high K+. , 1998, Circulation research.
[39] J. Marshall,et al. Hemorrhagic shock primes for increased expression of cytokine-induced neutrophil chemoattractant in the lung: role in pulmonary inflammation following lipopolysaccharide. , 1998, Journal of immunology.
[40] S. Opal,et al. Confirmatory interleukin-1 receptor antagonist trial in severe sepsis: a phase III, randomized, double-blind, placebo-controlled, multicenter trial. The Interleukin-1 Receptor Antagonist Sepsis Investigator Group. , 1997, Critical care medicine.
[41] R. Goris,et al. Inflammatory mediators in relation to the development of multiple organ failure in patients after severe blunt trauma. , 1995, Critical care medicine.
[42] S. Lowry,et al. Role of interleukin-1 and the therapeutic potential of interleukin-1 receptor antagonist in sepsis. , 1994, Circulatory shock.
[43] R. F. Johnston,et al. Recombinant Human Interleukin 1 Receptor Antagonist in the Treatment of Patients With Sepsis Syndrome: Results From a Randomized, Double-blind, Placebo-Controlled Trial , 1994 .
[44] R. Shenkar,et al. Hemorrhage and resuscitation induce alterations in cytokine expression and the development of acute lung injury. , 1994, American journal of respiratory cell and molecular biology.
[45] R. Sauerwein,et al. Cytokine Patterns in Patients After Major Vascular Surgery, Hemorrhagic Shock, and Severe Blunt Trauma Relation with Subsequent Adult Respiratory Distress Syndrome and Multiple Organ Failure , 1993, Annals of surgery.
[46] R. Shenkar,et al. Effects of hemorrhage on cytokine gene transcription. , 1993, Lymphokine and cytokine research.
[47] M. Glauser,et al. Septic shock: pathogenesis , 1991, The Lancet.
[48] E. Abraham,et al. Effects of hemorrhage on interleukin-1 production. , 1988, Circulatory shock.
[49] T. Petty,et al. Adult respiratory distress syndrome: risk with common predispositions. , 1983, Annals of internal medicine.
[50] K. Tracey,et al. IL-1alpha and IL-1beta are endogenous mediators linking cell injury to the adaptive alloimmune response. , 2007, Journal of immunology.
[51] K. Tracey,et al. Targeting high mobility group box 1 as a late-acting mediator of inflammation. , 2003, Critical care medicine.
[52] I. Chaudry,et al. Cytokine gene expression in splenic macrophages and Kupffer cells following haemorrhage. , 1995, Cytokine.
[53] A. Ellrodt,et al. Sepsis and septic shock. , 1986, Emergency medicine clinics of North America.