N-formyl methionine peptide-driven neutrophil activation in idiopathic inflammatory myopathies
Authors' conclusion
Our findings show that fMET-FPR1 signalling drives neutrophil activation in DM and IBM, promoting inflammation and muscle damage.
Study context
- Population
- Patients with IIM (dermatomyositis (DM) and inclusion body myositis (IBM)) and healthy controls
- Participants
- 46 / 40 / 40
- Comparison
- IBM and DM vs healthy controls
- IBMn = 46
- DMn = 40
- Healthy controlsn = 40reference
- Outcome
- Plasma fMET levels
Methodological detailscase-control, flow cytometry, ELISA
- Case-control
- Flow cytometry
- ELISA
Main finding
As reported in the abstract
Plasma fMET
DM vs Healthy controls: P < 0.0001 for DM · IBM vs Healthy controls: P = 0.0002 for IBM
Further findings
| Outcome | P value |
|---|---|
| Plasma calprotectinDM vs Healthy controls · elevated | P = 0.01 |
| NE-DNA complexesDM vs Healthy controls · increased | P = 0.03 |
| NE-DNA complexesIBM vs Healthy controls · increased | P < 0.0001 |
Correlation of fMET with MMT8 in antibody-negative IBM
- Inverse correlation, r
- −0.53
- P
- P = 0.02
Plasma calprotectin
- Not elevated in IBM
Plasma-induced neutrophil activation with FPR1 inhibition
- Significantly reduced in DM
- P < 0.0001
- Significantly reduced in IBM
- P = 0.0012
- Restoring CD66b and partially CD11b to control levels
Original publication
N-formyl methionine peptide-driven neutrophil activation in idiopathic inflammatory myopathies. Rheumatology (Oxford). Published 15 September 2025. doi:10.
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