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Vol. 52, Issue 3, 349-374, September 2000
Department of Pharmacology and Toxicology, Michigan State
University, East Lansing, Michigan
I. Introduction
II. General Mechanisms of Transendothelial Neutrophil Migration
A. Capture and Rolling
1. Leukocyte Selectin.
2. Platelet Selectin.
3. Endothelial Cell Selectin.
B. Firm Adhesion
1. Integrins.
2. Intercellular Adhesion Molecules.
C. Polymorphonuclear Leukocyte Homing to Transmigration Sites on
Endothelium
D. Transmigration
E. Migration as an Ordered Sequence of Events
F. Soluble Mediators of Migration
1. Cytokines: Tumor Necrosis Factor-
and Interleukin-1.
2. Chemoattractants.
a. Platelet-activating factor.
b. Leukotriene B4.
c. Complement protein C5a.
d. Formyl-methionyl-leucyl-phenylalanine.
e. Chemokines.
3. Cytokine-Chemoattractant Interaction during Migration.
G. Implications
III. Polymorphonuclear Leukocyte Migration in the Lungs
A. Marginated Pool of Polymorphonuclear Leukocytes
B. Site of Migration
C. Adhesion Molecule Requirements
1. Integrins.
2. Selectins.
D. Models of Pulmonary Polymorphonuclear Leukocyte Migration
1. Bacteria and Bacterial Products.
2. Acid Aspiration.
3. Interleukin-1.
4. Complement Protein C5a.
5. Immune-Complex Deposition.
6. Summary and Research Needs.
E. Polymorphonuclear Leukocyte Migration during Endotoxemia: A
Special Case of CD18 Inhibition?
IV. Pharmacologic Intervention
A. Lipid A Analogs
B. Cytokine Blockers
C. Steroids
D. Nonsteroidal Anti-Inflammatory Drugs
E. Anti-Selectin Therapies
1. Fucoidan.
2. Glycomimetics.
F. Anti-Integrin Therapies
1. Leumedins.
2. Ligand-Based Peptide Inhibitors.
G. 3-Hydroxy-3-methyl-glutaryl Coenzyme A Reductase Inhibitors
H. Nitric Oxide Donors
V. Summary
References
Leukocyte trafficking into pulmonary tissue and airspaces is a critical component of the host defense response. Activation and migration of polymorphonuclear leukocytes (PMNs) into lungs also contribute to inflammatory tissue injury and remodeling of tissue architecture. There have been considerable advances in our understanding of the mechanisms that control PMN adhesion and transendothelial migration (TEM). Mechanisms of migration unique to the lungs have been described with regard to the profile of adhesion molecules, cytokines, and chemokines elicited during PMN emigration from blood vessels. This work reviews general mechanisms of TEM of PMNs and discusses the nature of PMN recruitment in several models of airway inflammation that illustrate how various stimuli elicit different responses. Pharmacologic manipulation of adhesive interactions between PMNs and endothelial cells is a current area of research aimed at developing pharmacologic agents to control inflammation during pulmonary and other inflammatory diseases. A summary of some of these agents and their actions is presented.
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