Peter A. Ward

ORCID: 0000-0003-1285-8365
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About
Contact & Profiles
Research Areas
  • Immune Response and Inflammation
  • Complement system in diseases
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Cell Adhesion Molecules Research
  • Sepsis Diagnosis and Treatment
  • S100 Proteins and Annexins
  • Blood Coagulation and Thrombosis Mechanisms
  • Neonatal Respiratory Health Research
  • Respiratory Support and Mechanisms
  • Macrophage Migration Inhibitory Factor
  • Nitric Oxide and Endothelin Effects
  • Inflammasome and immune disorders
  • Heme Oxygenase-1 and Carbon Monoxide
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Cardiac Ischemia and Reperfusion
  • Monoclonal and Polyclonal Antibodies Research
  • Immune cells in cancer
  • Inflammatory mediators and NSAID effects
  • Inflammation biomarkers and pathways
  • Chemokine receptors and signaling
  • Antibiotics Pharmacokinetics and Efficacy
  • Receptor Mechanisms and Signaling
  • Immune Cell Function and Interaction
  • Eicosanoids and Hypertension Pharmacology
  • Erythrocyte Function and Pathophysiology

University of Warwick
2025

Dorset County Hospital
2025

University of Michigan
2015-2024

Massachusetts General Hospital
1973-2024

The University of Texas at Austin
1996-2023

Royal North Shore Hospital
1997-2023

Google (United States)
2022

British Dental Association
2019

Ann Arbor Center for Independent Living
1994-2018

British Antarctic Survey
1996-2017

Neutrophil-endothelial cell interactions are mediated by interacting sets of adhesion molecules (CAMs) and chemoattractant/activator to form an “adhesion cascade.” The initial phase inflammation, a transient slowing neutrophils in postcapillary venules, is selectins. Subsequently, firm the vessel wall occurs via interaction CD11/GD18 (β2) integrins endothelial ligands such as intercellular molecule-1 (ICAM-1). This binding requires activation exposure neutrophil variety...

10.1096/fasebj.8.8.8181668 article EN The FASEB Journal 1994-05-01

Human endothelial cells produced a neutrophil chemotactic factor (NCF) upon stimulation with tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), or lipopolysaccharide (LPS). The expression of cell-derived NCF messenger RNA and biological activity was both time- concentration-dependent. Maximal mRNA occurred at 10 2 nanograms per milliliter for TNF IL-1β, respectively; first observed 1 hour after maintained least 24 hours. In situ hybridization analysis showed that peaked in treated by...

10.1126/science.2648570 article EN Science 1989-03-17

In the present paper, we characterize an antibody, mAb BV13, directed to mouse vascular endothelial (VE)-cadherin, a major adhesive protein of interendothelial adherens junctions. When added cultured cells, BV13 induces redistribution VE-cadherin from intercellular did not change localization platelet cell adhesion molecule or tight junction markers such as zonula occludens 1, cingulin, and junctional molecule. Intravenous administration induced concentration- time-dependent increase in...

10.1073/pnas.96.17.9815 article EN Proceedings of the National Academy of Sciences 1999-08-17

Intravascular activation of the complement system with cobra venom factor results in acute lung injury, which has been quantitated by increases vascular permeability. Cobra preparations devoid phospholipase A2 activity retain full lung-damaging capacity. The injury is associated preceding appearance chemotactic serum coincident development a profound neutropenia. immunochemically related to human C5a. Morphologic studies have revealed discontinuities endothelial cell lining alveolar...

10.1172/jci110548 article EN Journal of Clinical Investigation 1982-05-01

Chemotactic factor-enriched butanol extracts from Escherichia coli culture filtrates were fractionated and purified by high pressure liquid chromatography. The yield individual fractions of biological activity (lysosomal enzyme secretion) antigenic (competition with [3H]fMet-Leu-Phe for binding to rabbit anti-fMet-Leu-Phe) revealed an average 50% recovery original material. Five peaks separated as demonstrated enzyme-releasing activity. Three these coincided exactly activity, suggesting that...

10.1016/s0021-9258(18)91029-x article EN cc-by Journal of Biological Chemistry 1984-05-01

Sepsis remains a serious cause of morbidity and mortality, the pathophysiology disease is not clear. The definition clinical manifestations sepsis ever evolving. This review discusses search for effective therapeutic interventions, hurdles in translational research, new therapies development current trials.

10.1172/jci200319523 article EN Journal of Clinical Investigation 2003-08-15

Human umbilical vein endothelial cells have recently been shown to respond C5a with increases in intracellular Ca2+, production of D-myo-inositol 1,4,5-triphosphate and superoxide anion generation. In the current studies, had found cause a time- dose-dependent manner rapid expression P-selectin, secretion von Willebrand factor, adhesiveness for human neutrophils. The effects P-selectin neutrophils were similar histamine thrombin on cells. C5a-stimulated endothelium was blocked by...

10.1172/jci117430 article EN Journal of Clinical Investigation 1994-09-01

During inflammation, neutrophils migrate from the vascular lumen into extravascular sites. In vitro assays have suggested that platelet-endothelial cell adhesion molecule-1 [PECAM-1 (CD31)], a member of immunoglobulin superfamily, is required for transmigration across endothelial monolayers. Antibody to human PECAM-1, which cross-reacts with rat was found block not only in vivo accumulation peritoneal cavity and alveolar compartment lung but also neutrophil skin grafts transplanted onto...

10.1126/science.8248808 article EN Science 1993-12-03
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