# The phenotype of monocyte subtypes and expression of chemokine receptors in the Chronic Venous Insufficiency

## TL;DR

This study shows how Chronic Venous Insufficiency affects monocyte subtypes and chemokine receptor expression, indicating a role in inflammation.

## Contribution

The study identifies specific changes in monocyte subtypes and chemokine receptor expression in Chronic Venous Insufficiency patients.

## Key findings

- CVI increases classical and non-classical monocytes while reducing intermediate monocytes.
- Non-classical monocytes show higher CCR5 expression in CVI patients.
- Classical monocytes exhibit lower CX3CR1 expression in CVI patients.

## Abstract

•Receptors have chemotactic property cells and are characterized as inflammatory markers.•Monocyte subtypes can play an important role in the Chronic Venous Disease scenario.•Receptors that act by recruiting monocytes include CCR2, CCR5, and CX3CR1.•Chronic Venous Insufficiency changes the monocyte phenotype.•The chemokine receptors might be changed by the Chronic Venous Insufficiency.

Receptors have chemotactic property cells and are characterized as inflammatory markers.

Monocyte subtypes can play an important role in the Chronic Venous Disease scenario.

Receptors that act by recruiting monocytes include CCR2, CCR5, and CX3CR1.

Chronic Venous Insufficiency changes the monocyte phenotype.

The chemokine receptors might be changed by the Chronic Venous Insufficiency.

The aim of this study was to evaluate monocyte subtypes and the chemokine receptors, comparing individuals with and without Chronic Venous Insufficiency (CVI).

The authors included patients undergoing surgery for varicose veins of the lower limbs (Classification of Venous Disorders – CEAP: C1‒C3).

There were increased levels of classical and non-classical monocytes in the case group and a reduction in intermediate monocytes. Besides, there was higher expression of CCR5 in the non-classical monocytes and lower expression of CX3CR1 in the classical monocytes in the case group.

The inflammatory process present in patients with CVI can modulate the monocyte phenotype and the expression of the chemokine receptors at the protein level.