This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Redl, H. Articles by Schlag, G. Search for Related Content PubMed PubMed Citation Articles by Redl, H. Articles by Schlag, G.

American Journal of Pathology, Vol 139, 461-466, Copyright © 1991 by American Society for Investigative Pathology

REGULAR ARTICLES

Expression of endothelial leukocyte adhesion molecule-1 in septic but not traumatic/hypovolemic shock in the baboon

H Redl, HP Dinges, WA Buurman, CJ van der Linden, JS Pober, RS Cotran and G Schlag
Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria.

Baboons were subjected to septic or traumatic/hypovolemic shock and their tissues were examined for the de novo expression of endothelial leukocyte adhesion molecule 1 (ELAM-1), using immunohistochemical techniques. In animals with septic shock induced with live Escherichia coli, there was widespread expression of ELAM-1, recognized by monoclonal antibodies H4/18 or ENA-1 in most tissues examined with strong staining in the lung, liver, and kidneys. Endothelial leukocyte adhesion molecule 1 expression was evident in capillaries, venules, small veins, arterioles, and arteries. In contrast, baboons with traumatic/hypovolemic shock had minimal levels of focal ELAM expression in all organs studied. Similarly evidence of neutrophil activation, measured by granulocyte elastase levels in the plasma was much more pronounced in animals with septic shock. The study documents that lipopolysaccharide (LPS)- and cytokine-induced endothelial activation occurs in vivo in septic shock. Much higher levels of ELAM-1 expression and plasma granulocyte-elastase titer in septic shock, as contrasted with traumatic/hypovolemic shock, are consistent with the higher levels of circulating tumor necrosis factor, other cytokines, and LPS in sepsis.

This article has been cited by other articles:

				J. S. POBER, M. S. KLUGER, and J. S. SCHECHNER Human Endothelial Cell Presentation of Antigen and the Homing of Memory/Effector T Cells to Skin Ann. N.Y. Acad. Sci., September 1, 2001; 941(1): 12 - 25. [Abstract] [Full Text] [PDF]

				B. Schleiffenbaum, J. Fehr, B. Odermatt, and R. Sperb Inhibition of Leukocyte Emigration Induced During the Systemic Inflammatory Reaction In Vivo Is Not Due to IL-8 J. Immunol., October 1, 1998; 161(7): 3631 - 3638. [Abstract] [Full Text] [PDF]

				S. KAYAL, J.-P. JAIS, N. AGUINI, J. CHAUDIERE, and J. LABROUSSE Elevated Circulating E-Selectin, Intercellular Adhesion Molecule 1, and von Willebrand Factor in Patients with Severe Infection Am. J. Respir. Crit. Care Med., March 1, 1998; 157(3): 776 - 784. [Abstract] [Full Text] [PDF]

				M. S. CARRAWAY, K. E. WELTY-WOLF, S. P. KANTROW, Y.-C. T. HUANG, S. G. SIMONSON, L. G. QUE, T. K. KISHIMOTO, and C. A. PIANTADOSI Antibody to E- and L-Selectin Does Not Prevent Lung Injury or Mortality in Septic Baboons Am. J. Respir. Crit. Care Med., March 1, 1998; 157(3): 938 - 949. [Abstract] [Full Text] [PDF]

				C. J. CUMMINGS, C. N. SESSLER, L. D. BEALL, B. J. FISHER, A. M. BEST, and A. A. FOWLER III Soluble E-Selectin Levels in Sepsis and Critical Illness . Correlation with Infection and Hemodynamic Dysfunction Am. J. Respir. Crit. Care Med., July 1, 1997; 156(2): 431 - 437. [Abstract] [Full Text]

				P. C. Ridings, S. Holloway, G. L. Bloomfield, M. L. Phillips, B. J. Fisher, C. R. Blocher, H. J. Sugerman, and A. A. Fowler III Protective role of synthetic sialylated oligosaccharide in sepsis-induced acute lung injury J Appl Physiol, February 1, 1997; 82(2): 644 - 651. [Abstract] [Full Text] [PDF]