# Cross-sectional analysis of wound-associated soluble factors in early, established, and chronic wounds of recessive dystrophic epidermolysis bullosa patients

**Authors:** Vitali Alexeev, Leonie Huitema, Taylor Phillips, Paras Patel, Mauricio Salas Garza, Franziska Ringpfeil, Julio Cesar Salas-Alanis, Olga Igoucheva

PMC · DOI: 10.1007/s00403-025-04293-w · Archives of Dermatological Research · 2025-06-04

## TL;DR

This study analyzes wound fluid from RDEB patients to identify soluble factors that may hinder healing and could be targeted for treatment.

## Contribution

The study identifies unique patterns of pro-inflammatory and growth factors in RDEB wounds compared to other chronic wounds.

## Key findings

- Proinflammatory CXCL8 and IL-1β accumulate in established RDEB lesions.
- IL-17, IL-18, and IL-10 levels are significantly higher in RDEB chronic wounds than in venous ulcers.
- VEGF, G-CSF, and HGF growth factors are elevated in RDEB wounds compared to other chronic wounds.

## Abstract

Poorly healing wounds represent the primary health-related burden for hereditary recessive dystrophic epidermolysis bullosa (RDEB) patients. Contribution of wound-associated soluble constituents to wound progression remains not well defined.

To conduct cross-sectional analysis of cytokine, chemokine, and growth factor in exudates from RDEB wounds and define changes associated with wound progression.

Concentrations of selected cytokines, chemokines, and growth factors were evaluated by multiplex ELISA in eight blister fluids and 66 exudates from early, established, and chronic RDEB and five chronic venous ulcers (VU). A cross-sectional analysis was performed.

Our data demonstrated that proinflammatory CXCL8 and IL-1β tend to accumulate in established RDEB lesions. The levels of several interleukins including IL-17, IL-18, and IL-10 were significantly higher in RDEB chronic wounds than in VU. Contrary to VU and other chronic wounds, high levels of VEGF, G-CSF, and HGF growth factors were detected in RDEB established and chronic skin lesions.

Although this study is limited to cross-sectional analysis of wound exudates, detected high levels of specific pro-inflammatory, neutrophil-recruiting, and pro-angiogenic and pro-proliferative factors, such as IL-1β, CXCL8, VEGF, G-CSF, and HGF define RDEB wounds and offer potential pharmacological targets to improve wound healing in the patients.

The online version contains supplementary material available at 10.1007/s00403-025-04293-w.

## Linked entities

- **Proteins:** CXCL8 (C-X-C motif chemokine ligand 8), IL1B (interleukin 1 beta), IL17A (interleukin 17A), IL18 (interleukin 18), IL10 (interleukin 10), VEGFA (vascular endothelial growth factor A), CSF3 (colony stimulating factor 3), HGF (hepatocyte growth factor)
- **Diseases:** recessive dystrophic epidermolysis bullosa (MONDO:0009179)

## Full-text entities

- **Genes:** IL18 (interleukin 18) [NCBI Gene 3606] {aka IGIF, IL-18, IL-1g, IL1F4}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, CSF3 (colony stimulating factor 3) [NCBI Gene 1440] {aka C17orf33, CSF3OS, GCSF}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, HGF (hepatocyte growth factor) [NCBI Gene 3082] {aka DFNB39, F-TCF, HGFB, HPTA, SF}
- **Diseases:** VU (MESH:D014647), RDEB (MESH:D016108), chronic wounds (MESH:D014947), hereditary recessive dystrophic epidermolysis bullosa (MESH:D009386), chronic skin lesions (MESH:D012871), inflammatory (MESH:D007249)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12137523/full.md

## References

2 references — full list in the complete paper: https://tomesphere.com/paper/PMC12137523/full.md

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Source: https://tomesphere.com/paper/PMC12137523