# Profiles of Monocyte Subsets and Fibrosis-Related Genes in Patients with Muscular Dystrophy Undergoing Intermittent Prednisone Therapy

**Authors:** Asma Chikhaoui, Dorra Najjar, Sami Bouchoucha, Rim Boussetta, Nadia Ben Achour, Kalthoum Tizaoui, Ichraf Kraoua, Ilhem Turki, Houda Yacoub-Youssef

PMC · DOI: 10.3390/ijms26135992 · International Journal of Molecular Sciences · 2025-06-22

## TL;DR

This study explores how intermittent prednisone therapy affects monocyte subsets and fibrosis-related genes in muscular dystrophy patients.

## Contribution

The study identifies changes in monocyte profiles and fibrosis-related gene expression due to intermittent prednisone use in muscular dystrophy.

## Key findings

- Intermittent prednisone increases classical monocytes and decreases non-classical monocytes with anti-inflammatory markers.
- Twenty-one fibrosis-related genes, including CEBPB, are altered in dystrophic muscle biopsies.
- Classical monocytes and CEBPB may promote collagen 1 production, affecting monocyte/macrophage function.

## Abstract

Muscle dystrophies are a group of genetic disorders characterized by progressive muscle degeneration. Prednisone is a glucocorticoid drug widely used to prevent muscle weakness in these diseases. Despite its known beneficial role, the effect of intermittent delivery on monocytes’ polarization and on dystrophic muscle microenvironment has not yet been thoroughly investigated. In this study, our aim was to identify the phenotype of monocyte subsets in blood and the expression of fibrosis-related genes in dystrophic muscle biopsies in patients receiving intermittent prednisone therapy. We found an increased rate of classical monocytes and a decreased rate of non-classical monocytes that expressed anti-inflammatory marker CD206 in treated patients. In dystrophic muscles, 21 fibrosis-related genes were altered, among which we identified CCAAT/enhancer-binding protein beta CEBPB. Both classical monocytes and CEBPB are known for their roles in stimulating collagen 1 production, a probable marker hampering monocyte/macrophage function. Hence, in some patients with muscular dystrophy, intermittent prednisone treatment could shift the monocytes’ phenotype toward an M2, senescent-like profile. This seems to decrease the inflammatory infiltrate in muscle tissue, an observation that needs to be further confirmed.

## Linked entities

- **Genes:** CEBPB (CCAAT enhancer binding protein beta) [NCBI Gene 1051]
- **Proteins:** MRC1 (mannose receptor C-type 1)
- **Chemicals:** prednisone (PubChem CID 5865)
- **Diseases:** muscular dystrophy (MONDO:0020121)

## Full-text entities

- **Genes:** MRC1 (mannose receptor C-type 1) [NCBI Gene 4360] {aka CD206, CLEC13D, CLEC13DL, MMR, MRC1L1, bA541I19.1}, CEBPB (CCAAT enhancer binding protein beta) [NCBI Gene 1051] {aka C/EBP-beta, IL6DBP, NF-IL6, TCF5}
- **Diseases:** Fibrosis (MESH:D005355), genetic disorders (MESH:D030342), muscle weakness (MESH:D018908), muscle degeneration (MESH:D009410), dystrophic muscle (MESH:D019042), Muscle dystrophies (MESH:D009136), inflammatory (MESH:D007249)
- **Chemicals:** Prednisone (MESH:D011241)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

99 references — full list in the complete paper: https://tomesphere.com/paper/PMC12250195/full.md

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Source: https://tomesphere.com/paper/PMC12250195