<i>Staphylococcus aureus</i> toxins mediate endothelial Thrombomodulin release during severe invasive infections.

ABSTRACT: Thrombomodulin (TM) is a membrane protein with significant roles in coagulation hemostasis and immune response. Its soluble form (sTM) has recently emerged as a key biomarker for severe invasive bacterial infections, including Necrotizing Soft Tissue Infections (NSTI). While various mechanical, chemical, and enzymatic mechanisms have been linked to TM shedding, this study investigates the direct impact of bacterial stimuli on soft tissue cells as primary sources of TM release. We stimulated organotypic models, composed of fibroblast and endothelial cells, with NSTI clinical isolates and found that while Group A Streptococcus and Escherichia coli had minimal effect on TM release, Staphylococcus aureus infection triggered a significant increase of sTM levels. We further assesse

SUBMITTER: Seidner L 

PROVIDER: S-EPMC12721087 | biostudies-literature | 2026 Dec

REPOSITORIES: biostudies-literature