Abstract

Acid aspiration is recognized as a common clinically encountered amplifier of lung injury. In this proposal the investigators focus on the stimulated secretion of inflammatory mediators by alveolar macrophages and phenotype changes in endothelial cells that promote neutrophil adhesion. The mutual interactions of endothelial cells complement and leukocytes are carefully dissected in vitro and reverified by experiments conducted in vivo.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
5R01GM024891-19
Application #
2391848
Study Section
Surgery, Anesthesiology and Trauma Study Section (SAT)
Project Start
1977-07-01
Project End
2000-03-31
Budget Start
1997-04-01
Budget End
1998-03-31
Support Year
19
Fiscal Year
1997
Total Cost
Indirect Cost

  Institution

Name
Harvard University
Department
Surgery
Type
Schools of Medicine
DUNS #
082359691
City
Boston
State
MA
Country
United States
Zip Code
02115

  Publications

Kyriakides, C; Austen Jr, W G; Wang, Y et al. (2001) Mast cells mediate complement activation after acid aspiration. Shock 16:21-4
Kyriakides, C; Wang, Y; Austen Jr, W G et al. (2001) Sialyl Lewis(x) hybridized complement receptor type 1 moderates acid aspiration injury. Am J Physiol Lung Cell Mol Physiol 281:L1494-9
Kyriakides, C; Austen Jr, W; Wang, Y et al. (2000) Endothelial selectin blockade attenuates lung permeability of experimental acid aspiration. Surgery 128:327-31
Kyriakides, C; Austen Jr, W G; Wang, Y et al. (2000) Neutrophil mediated remote organ injury after lower torso ischemia and reperfusion is selectin and complement dependent. J Trauma 48:32-8
Williams, J P; Pechet, T T; Weiser, M R et al. (1999) Intestinal reperfusion injury is mediated by IgM and complement. J Appl Physiol 86:938-42
Kyriakides, C; Austen Jr, W; Wang, Y et al. (1999) Membrane attack complex of complement and neutrophils mediate the injury of acid aspiration. J Appl Physiol 87:2357-61
Furman, M I; Benoit, S E; Barnard, M R et al. (1998) Increased platelet reactivity and circulating monocyte-platelet aggregates in patients with stable coronary artery disease. J Am Coll Cardiol 31:352-8
Hastie, L E; Patton, W F; Hechtman, H B et al. (1998) Metabolites of the phospholipase D pathway regulate H2O2-induced filamin redistribution in endothelial cells. J Cell Biochem 68:511-24
Shojaee, N; Patton, W F; Chung-Welch, N et al. (1998) Expression and subcellular distribution of filamin isotypes in endothelial cells and pericytes. Electrophoresis 19:323-32
Peyton, B D; Rohrer, M J; Furman, M I et al. (1998) Patients with venous stasis ulceration have increased monocyte-platelet aggregation. J Vasc Surg 27:1109-15;discussion 1115-6

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