Burn-Related Glycocalyx Derangement and the Emerging Role of MMP8 in Syndecan Shedding.

Summary

Serum profiling of 28 burn patients combined with scRNA-seq and microarray analyses revealed upregulated MMP8 associated with glycocalyx shedding and inhalation injury. Exogenous MMP8 induced glycocalyx loss in human lung epithelial models, implicating MMP8 as a mediator of post-burn lung injury and a potential therapeutic target.

Key Findings

• Burn patient sera showed elevated shed glycocalyx components and MMP8, correlating with inhalation injury.
• scRNA-seq and microarray revealed upregulation of immune cell–derived degrading enzymes, especially MMP8.
• MMP8 treatment of human in vitro lung tissue models induced glycocalyx shedding in alveolar epithelial cells.

Clinical Implications

MMP8 and shed glycocalyx components could serve as biomarkers of lung injury risk after burns; MMP8 inhibition merits evaluation to mitigate post-burn lung injury including ARDS.

Limitations

• Small cohort size (N=28) limits generalizability
• Observational correlations without in vivo inhibition studies to establish causality

Future Directions

Validate MMP8–glycocalyx links in larger cohorts and in vivo burn models; test MMP8 inhibitors and develop shedding biomarkers for risk stratification.