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Updated: Jul 5, 2026
Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
In vivo transmigrated monocytes from patients with stable coronary artery disease have a reduced expression of CD11b
J M Paulsson1, E Dadfar, C Held
1Department of Clinical Immunology, Karolinska University Hospital, Stockholm, Sweden.
Insights
Monocytes in coronary artery disease (CAD) patients show reduced CD11b expression after migrating to inflammation sites. This suggests altered monocyte transmigration contributes to CAD progression.
Area of Science:
- Cardiovascular Science
- Immunology
- Cell Biology
Background:
- Coronary artery disease (CAD) involves monocyte-derived cells infiltrating vessel walls.
- Altered monocyte transmigration may contribute to this cellular accumulation in CAD.
Purpose of the Study:
- To investigate differences in monocyte transmigration in patients with stable CAD compared to controls.
- To examine monocyte adhesion molecule expression and mobilization following in vivo transmigration.
Main Methods:
- Utilized the skin blister method to collect in vivo transmigrated cells from local inflammation sites.
- Enrolled 19 patients with stable CAD and 19 matched controls.
- Assessed inflammatory markers, chemokine gradients, and adhesion molecule expression (CD11b, VLA-4) on peripheral and transmigrated monocytes.
Main Results:
- Peripheral monocyte expression of CD11b and VLA-4 did not differ between CAD patients and controls.
- In vivo transmigrated monocytes from CAD patients exhibited significantly reduced CD11b expression and mobilization.
- This CD11b alteration in transmigrated monocytes could not be replicated in vitro.
Conclusions:
- Monocyte transmigration processes are altered in patients with coronary artery disease.
- Reduced CD11b expression and mobilization on transmigrated monocytes may play a role in CAD pathogenesis.
- These findings highlight differences in monocyte behavior at inflammatory sites in CAD patients.
Abstract:
Coronary artery disease (CAD) is characterized by infiltration of monocyte derived cells in the intima of the vessel wall. We hypothesized that accumulation of these cells is caused partly by an altered monocyte transmigration process in CAD. To gain insight into this issue we applied the skin blister method that allows collection of in vivo transmigrated cells at sites of local inflammation. Nineteen patients with stable CAD and 19 matched controls were enrolled. Markers of inflammation and gradients of chemokines, as well as adhesion molecule expression and up-regulation capacity, were studied. The expression of inflammatory markers, such as C-reactive protein, interleukin (IL)-6, tumour necrosis factor-alpha and IL-10, was similar in patients and controls, indicating that patients were in a stable phase of the disease. Expression of adhesion molecules, CD11b and very late activation antigen-4, on peripheral monocytes did not differ between patients and controls. However, following in vivo transmigration, monocytes in patients with CAD had a significantly reduced expression and mobilization of CD11b. The effect on CD11b could not be reproduced by in vitro stimulation with blister fluid, representing a local inflammatory milieu, or in an in vitro system of transmigration. These findings point towards differences in monocyte CD11b expression and availability at an inflammatory site between patients with CAD and healthy controls.
