Related Experiment Videos
Endogenous mediators that inhibit the leukocyte-endothelium interaction
1Department of Biochemical Pharmacology, William Harvey Research Institute, London, UK.
Trends in Pharmacological Sciences
|January 14, 1998
Summary
This review explores how the body naturally reduces leukocyte extravasation, focusing on inhibitory mechanisms. Understanding these pathways could lead to new anti-inflammatory therapies for conditions like asthma.
Area of Science:
- Immunology
- Cell Biology
- Pharmacology
Background:
- Leukocyte extravasation is crucial in inflammation, neoplasia, and asthma.
- Initial steps involve cell-adhesion molecules and cytokines at the post-capillary venule.
- Mechanisms downregulating extravasation are less understood.
Purpose of the Study:
- To review inhibitory mechanisms of leukocyte extravasation.
- To highlight the role of endogenous mediators in downregulating leukocyte-endothelium interactions.
- To explore potential anti-inflammatory therapeutic targets.
Main Methods:
- Review of existing literature on leukocyte extravasation.
- Focus on inhibitory pathways and endogenous mediators.
- Utilizes neutrophilic polymorphonuclear leukocytes as a model.
Main Results:
- Established roles of adhesion molecules and cytokines in initiating extravasation.
- Identified endogenous mediators like adenosine, lipocortin 1, NO, prostacyclin, and cathepsin G as key downregulators.
- Highlighted the potential for novel anti-inflammatory therapies based on these inhibitory mechanisms.
Conclusions:
- Understanding endogenous downregulation of leukocyte extravasation is critical.
- Inhibitory mechanisms offer promising targets for novel anti-inflammatory drug development.
- Further research into mediators like adenosine and lipocortin 1 could yield therapeutic benefits.