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Updated: Aug 13, 2026
Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice
Published on: August 13, 2015
Dexamethasone inhibits leukocyte emigration in rat mesenteric post-capillary venules: an intravital microscopy study
A Tailor1, R J Flower, M Perretti
1Department of Biochemical Pharmacology, The William Harvey Research Institute, London, United Kingdom.
Insights
Dexamethasone selectively inhibits leukocyte emigration, but not adhesion, in response to IL-1beta and PAF. This anti-inflammatory effect is dose-dependent and more pronounced on emigration than adhesion.
Area of Science:
- Pharmacology
- Immunology
- Inflammation Research
Background:
- Leukocyte-endothelial interactions are critical in inflammatory responses.
- Interleukin-1beta (IL-1beta) and platelet-activating factor (PAF) are key mediators of inflammation.
- Dexamethasone (DEX) is a potent anti-inflammatory corticosteroid.
Purpose of the Study:
- To investigate the effect of dexamethasone on IL-1beta and PAF-induced leukocyte-endothelial interactions.
- To determine whether DEX preferentially inhibits leukocyte adhesion or emigration.
Main Methods:
- Subcutaneous administration of DEX to rats.
- Induction of leukocyte-endothelial interactions using IL-1beta and PAF in the rat mesenteric post-capillary venules.
- Quantification of leukocyte extravasation and adhesion.
Main Results:
- DEX dose-dependently inhibited IL-1beta-induced leukocyte extravasation (ED50 = 40 microg/kg).
- DEX partially inhibited IL-1beta-induced leukocyte adhesion (ED50 = 480 microg/kg).
- DEX inhibited PAF-induced leukocyte emigration but not adhesion, increasing emigration time.
Conclusions:
- Dexamethasone preferentially inhibits leukocyte emigration over adhesion.
- The anti-inflammatory effects of DEX are more pronounced on the emigration process.
- These findings highlight a selective mechanism of action for DEX in modulating inflammatory cell trafficking.
Abstract:
The effect of subcutaneous administration of dexamethasone (DEX) on interleukin-1beta(IL-1beta, 20 ng i.p., - 2 h) and platelet-activating factor (PAF, 100 nM in superfusion) -induced leukocyte interaction with the endothelium of rat mesenteric post-capillary venules was studied. DEX produced a dose-dependent inhibition of IL-1beta-induced leukocyte extravasation in the rat mesenteric vascular bed, with a calculated ED5o of 40 microg/kg and a maximal effect of 80-100% inhibition at 0.1 mg/kg. IL-1beta-induced cell adhesion to post-capillary venules was only partially inhibited by the steroid, with a calculated ED50 of 480 microg/kg and a maximal effect of 40-60% inhibition. Furthermore, the steroid inhibited leukocyte emigration, but not adhesion, caused by superfusion of the mesenteric vascular bed with PAF. A doubling of leukocyte emigration time (from 226 to 552 s) was observed after treatment of rats with DEX. Administration for 5 days of a dose of 10 microg/kg DEX (which was inactive when given as a single injection) resulted again in a selective inhibition of IL-1beta-induced leukocyte emigration, without effect on cell adhesion. These data demonstrate a preferential susceptibility of the leukocyte emigration process to the inhibitory action of DEX.
