Related Experiment Video
Updated: Jul 17, 2026
12:55
A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
Published on: December 9, 2021
Carbon monoxide-releasing molecules modulate leukocyte-endothelial interactions under flow
Paula Urquhart1, Guglielmo Rosignoli, Dianne Cooper
1William Harvey Research Institute, London, UK.
The Journal of Pharmacology and Experimental Therapeutics
|February 10, 2007
Summary
Carbon monoxide-releasing molecule 3 (CORM-3) reduces acute inflammation by inhibiting neutrophil activation and rolling on blood vessel walls. This anti-inflammatory effect is linked to potassium channel opening.
Area of Science:
- Biomedical Science
- Pharmacology
- Immunology
Background:
- Carbon monoxide (CO) from heme oxygenase has known biological effects.
- CO-releasing molecules (CO-RMs) offer a way to study CO's therapeutic potential.
- Leukocyte-endothelial interactions are key in inflammatory responses.
Purpose of the Study:
- To investigate if CO from a CO-releasing molecule (CORM-3) can modulate leukocyte-endothelial interactions.
- To assess the anti-inflammatory effects of CORM-3 in vivo and in vitro.
- To elucidate the mechanism of action for CORM-3's anti-inflammatory properties.
Main Methods:
- Tested CORM-3 in two acute inflammation models in vivo.
- Performed in vitro static experiments on neutrophil and endothelial cell adhesion molecules.
- Studied polymorphonuclear neutrophil (PMN) interactions with human umbilical vein endothelial cells (HUVECs).
Main Results:
- CORM-3 demonstrated significant anti-inflammatory effects in vivo, reducing neutrophil extravasation.
- In vitro, CORM-3 inhibited PMN CD11b up-regulation and L-selectin shedding.
- CORM-3 inhibited PMN capture and rolling on HUVECs, with effects potentially mediated by potassium channel opening.
Conclusions:
- CORM-3 exhibits acute anti-inflammatory effects in vivo.
- These effects are likely due to targeting PMN activation and rolling on the endothelium.
- The mechanism may involve the modulation of potassium channels in neutrophils.
Related Concept Videos
01:24Regulation of Angiogenesis and Blood Supply
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
01:26Acute Inflammation II: Cellular Phase
The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
01:28Nitric Oxide Signaling Pathway
Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...