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Single-cell transcriptome reveals Staphylococcus aureus modulating fibroblast differentiation in the bone-implant

Jinlong Yu¹, Boyong Wang¹, Feiyang Zhang¹

¹Department of Orthopedics, Shanghai Sixth People's Hospital, No. 600, Yi Shan Road, Shanghai, 200233, China.

Molecular Medicine (Cambridge, Mass.)

|March 17, 2023

Summary

Bone-implant interface fibroblasts exhibit distinct responses to infection. Study identifies CTHRC1+ fibroblasts and key regulators driving pro-inflammatory or matrix-producing phenotypes in periprosthetic joint infection.

Keywords:

Fibroblast Implant-associated infection Staphylococcus aureus scRNA-seq

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Area of Science:

Biomedical Engineering
Cell Biology
Immunology

Background:

Investigating cellular heterogeneity at the bone-implant interface is crucial for understanding implant-associated infections.
Fibroblast behavior significantly impacts outcomes in periprosthetic joint infection (PJI) and aseptic loosening (AL).

Approach:

Single-cell RNA sequencing (scRNA-seq) was performed on human periprosthetic tissues from PJI and AL patients.
Integrated publicly available datasets to identify disease-specific fibroblast subtypes and regulatory networks.
Utilized pseudotime trajectory and SCENIC analyses to pinpoint transcription regulators of fibroblast differentiation.

Key Points:

Identified eight major cell types in the bone-implant interface, with CTHRC1+ fibroblasts being prominent.
Discovered distinct fibroblast differentiation into pro-inflammatory (PJI) and matrix-producing (AL) phenotypes.
NPAS2 and TFEC were implicated in PJI-associated pro-inflammatory fibroblast polarization, while HMX1, SOX5, SOX9, ZIC1, ETS2, and FOXO1 regulate matrix production.

Conclusions:

Discovered CTHRC1+ fibroblasts in the bone-implant interface.
Revealed a bipolar fibroblast differentiation mode, suggesting infection drives pro-inflammatory phenotypes via NPAS2 and TFEC.