Monocyte state 1 (MS1) cells in critically ill patients with sepsis or non-infectious conditions: association with disease course and host response
Authors' conclusion
High MS1 cell percentages are associated with increased disease severity and shock in critically ill patients with sepsis or a non-infectious condition.
Study context
- Population
- Intensive care unit (ICU) patients with sepsis, compared with ICU patients without infection and healthy controlssepsis
- Participants
- 332 patients
- Exposure
- Low vs intermediate vs high MS1 cell levels
- ICU patients without infectionn = 215
- Outcome
- Association of MS1 cell levels with disease presentation, outcomes and host response
Methodological detailstranscriptome deconvolution (CIBERSORTx), gene co-expression network and gene set enrichment analyses, 15 plasma biomarkers
- Transcriptome deconvolution (CIBERSORTx)
- Gene co-expression network and gene set enrichment analyses
- 15 plasma biomarkers
Main finding
As reported in the abstract
- MS1 groups did not differ in demographics or comorbidities
- Intermediate and high MS1 groups had higher disease severity and more often shock
- MS1 cell abundance did not differ between survivors and non-survivors, or by acquisition of secondary infection
- Higher MS1 % associated with downregulation of lymphocyte-related and interferon response genes and upregulation of inflammatory pathways, incl. TNF signalling via NF-κB
- MS1 % positively correlated with quantitative sepsis response signature and molecular degree of perturbation scores; transcriptomic subtypes differed in MS1 abundance
- Plasma biomarkers of inflammation, endothelial and coagulation activation largely similar between MS1 groups
Observational data: associations, not effects.
Further findings
ICU patients without infection
- MS1 % and relation with disease severity, shock and host response dysregulation highly similar to sepsis
Original publication
Monocyte state 1 (MS1) cells in critically ill patients with sepsis or non-infectious conditions: association with disease course and host response. Crit Care. Published 19 March 2024. doi:10. 1186/ s13054-024-04868-5
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