Protection from septic shock by neutralization of macrophage migration inhibitory factor (original) (raw)

• Glauser, M. P., Zanetti, G., Baumgartner, J. D. & Cohen, J. Septic shock: pathogenesis. Lancet 338, 732–736 (1991).
  Article CAS Google Scholar
• Abraham, E. Why immunomodulatory therapies have not worked in sepsis? Intensive Care Med. 25, 556–566 ( 1999).
  Article CAS Google Scholar
• Bloom, B. R. & Bennett, B. Mechanism of a reaction in vitro associated with delayed-type hypersensitivity. Science 153, 80–82 (1966).
  Article CAS Google Scholar
• David, J. Delayed hypersensitivity in vitro: its mediation by cell-free substances formed by lymphoid cell-antigen interaction. Proc.Natl.Acad.Sci.USA 56, 72–77 ( 1966).
  Article CAS Google Scholar
• Nathan, C. F., Remold, H. G. & David, J.R. Characterization of a lymphocyte factor which alters macrophage function. J. Exp. Med. 137, 275 –288 (1973).
  Article CAS Google Scholar
• Nathan, C. F., Karnovsky, M. L. & David, J.R. Alterations of macrophage functions by mediators from lymphocytes. J. Exp. Med. 133, 1356– 1376 (1971).
  Article CAS Google Scholar
• Bernhagen, J. et al. MIF is a pituitary-derived cytokine that potentiates lethal endotoxaemia. Nature 365, 756– 759 (1993).
  Article CAS Google Scholar
• Calandra, T. et al. MIF as a glucocorticoid-induced modulator of cytokine production . Nature 377, 68–71 (1995).
  Article CAS Google Scholar
• Calandra, T., Spiegel, L. A., Metz, C. N. & Bucala, R. Macrophage migration inhibitory factor (MIF) is a critical mediator of the activation of immune cells by exotoxins of Gram-positive bacteria. Proc.Natl.Acad.Sci.USA 95, 11383–11388 (1998).
  Article CAS Google Scholar
• Calandra, T., Bernhagen, J., Mitchell, R. A. & Bucala, R. The macrophage is an important and previously unrecognized source of macrophage migration inhibitory factor. J. Exp. Med. 179, 1895–1902 (1994).
  Article CAS Google Scholar
• Bernhagen, J. et al. Purification, bioactivity, and secondary structure analysis of mouse and human macrophage migration inhibitory factor (MIF). Biochemistry 33, 14144–14155 (1994).
  Article CAS Google Scholar
• Bacher, M. et al. An essential regulatory role for macrophage migration inhibitory factor in T-cell activation. Proc. Natl. Acad. Sci. USA 93, 7849–7854 (1996).
  Article CAS Google Scholar
• Mitchell, R. A., Metz, C. N., Peng, T. & Bucala, R. Sustained mitogen-activated protein kinase (MAPK) and cytoplasmic phopholipase A2 activation by macrophage migration inhibitory factor (MIF). J.Biol.Chem. 274 , 18100–18106 (1999).
  Article CAS Google Scholar
• Lan, H.Y. et al. The pathogenic role of macrophage migration inhibitory factor in immunologically induced kidney disease in the rat. J. Exp. Med. 185, 1455–1465 ( 1997).
  Article CAS Google Scholar
• Mikulowska, A., Metz, C. N., Bucala, R. & Holmdahl, R. Macrophage migration inhibitory factor is involved in the pathogenesis of collagen type II-induced arthritis in mice. J. Immunol. 158, 5514 –5517 (1997).
  CAS Google Scholar
• Leech, M. et al. Involvement of macrophage migration inhibitory factor in the evolution of rat adjuvant arthritis. Arthritis Rheum. 41, 910–917 (1998).
  Article CAS Google Scholar
• Lan, H. Y. et al. Macrophage migration inhibitory factor expression in human renal allograft rejection. Transplantation 16, 1465–1471 (1998).
  Article Google Scholar
• Donnelly, S. C. et al. Regulatory role for macrophage migration inhibitory factor in acute respiratory distress syndrome. Nat. Med. 3 , 320–323 (1997).
  Article CAS Google Scholar
• Bacher, M. et al. MIF expression in experimentally-induced endotoxemia. Am. J. Pathol. 150, 235–246 (1997).
  CAS Google Scholar
• Bozza, M. et al. Targeted disruption of migration inhibitory factor gene reveals its critical role in sepsis. J. Exp. Med. 189, 341–346 (1999).
  Article CAS Google Scholar
• Marschall, J. C. & Creery, D. Pre-clinical models of sepsis. Sepsis 2, 187– 197 (1998).
  Article Google Scholar
• Cohen, J. & Abraham, E. Microbiologic findings and correlations with serum tumor necrosis factor-α in patients with severe sepsis and septic shock. J. Infect. Dis. 180, 116– 121 (1999).
  Article CAS Google Scholar
• Friedman, G., Silva, E. & Vincent, J.L. Has the mortality of septic shock changed with time? Crit. Care Med. 26, 2078– 2086 (1998).
  Article CAS Google Scholar
• Zanetti, G. et al. Cytokine production after intravenous or peritoneal gram-negative bacterial challenge in mice. Comparative protective efficacy of antibodies to tumor necrosis factor-α and to lipopolysaccharide. J. Immunol. 148, 1890–1897 (1992).
  CAS Google Scholar
• Echtenacher, B., Falk, W., Männel, D. N. & Krammer, P.H. Requirement of endogenous tumor necrosis factor/cachectin for recovery from experimental peritonitis. J. Immunol. 145, 3762–3766 (1990).
  CAS Google Scholar
• Heumann, D. et al. Contribution of TNF/TNF receptor and of Fas ligand to toxicity in murine models of endotoxemia and bacterial peritonitis. J. Inflamm. 47, 173–179 ( 1999).
  Google Scholar
• American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit. Care Med. 20, 864–874 (1992).
• Bagby, G. J., Plessala, K. J., Wilson, L. A., Thompson, K. J. & Nelson, S. Divergent efficacy of antibody to tumor necrosis factor-α in intravascular and peritonitis models of sepsis. J. Infect. Dis. 163, 83 –88 (1991).
  Article CAS Google Scholar
• Wang, H. et al. HMG-1 as a late mediator of endotoxin lethality in mice. Science 285, 248–251 ( 1999).
  Article CAS Google Scholar
• Maurer, M. et al. The c-kit ligand, stem cell factor, can enhance innate immunity through effects on mast cells. J. Exp. Med. 188, 2343–2348 (1991).
  Article Google Scholar
• Pfeffer, K. et al. Mice deficient for the 55kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succumb to L. monocytogenes infection . Cell 73, 457–467 (1993).
  Article CAS Google Scholar
• Rothe, J. et al. Mice lacking the tumor necrosis factor receptor 1 are resistant to TNF-mediated toxicity but highly susceptible to infection by Listeria monocytogenes. Nature 364, 798– 802 (1993).
  Article CAS Google Scholar
• Porat, R., Clark, B. D., Wolff, S. M. & Dinarello, C.A. Enhancement of growth of virulent strains of Escherichia coli by interleukin-1 . Science 254, 430–432 (1991).
  Article CAS Google Scholar
• Pasparakis, M., Alexopoulou, L., Episkopou, V. & Kollias, G. Immune and inflammatory responses in TNFα-deficient mice: a critical requirement for TNFα in the formation of primary B cell follicles, follicular dendritic cell networks and germinal centers, and in the maturation of the humoral immune response. J. Exp. Med. 184, 1397–1411 (1996).
  Article CAS Google Scholar
• Baumgartner, J. D. et al. Association between protective efficacy of anti-lipopolysaccharide (LPS) antibodies and suppression of LPS-induced tumor necrosis factor α and interleukin 6. Comparison of O side chain-specific antibodies with core LPS antibodies. J. Exp. Med. 171, 889– 896 (1990).
  Article CAS Google Scholar
• Kohler, J. et al. IFN-gamma involvement in the severity of Gram-negative infections in mice. J. Immunol. 151, 916– 921 (1993).
  CAS Google Scholar