Skip to main content

Daily Sepsis Research Analysis

3 papers

Three studies advance sepsis science across settings: a multicenter Ugandan proteomics analysis delineates an immunosuppressive host-response signature specific to malarial sepsis; a multi-omics mouse-to-human study proposes an early serum metabolite model (IC3) for sepsis-associated acute kidney injury; and a prehospital evaluation shows PRESEP as the only model outperforming unaided EMS assessment for identifying ED Sepsis-3 cases.

Summary

Three studies advance sepsis science across settings: a multicenter Ugandan proteomics analysis delineates an immunosuppressive host-response signature specific to malarial sepsis; a multi-omics mouse-to-human study proposes an early serum metabolite model (IC3) for sepsis-associated acute kidney injury; and a prehospital evaluation shows PRESEP as the only model outperforming unaided EMS assessment for identifying ED Sepsis-3 cases.

Research Themes

  • Host-response proteomics and stratification in sepsis
  • Early biomarkers and multi-omics for sepsis-associated acute kidney injury
  • Prehospital sepsis prediction and EMS decision support

Selected Articles

1. Host Response Stratification in Malarial and Non-malarial Sepsis: A Prospective, Multicenter Analysis From Uganda.

78.5Level IIICohortCritical care medicine · 2025PMID: 39937058

Across two Ugandan cohorts, malarial and non-malarial sepsis shared a largely conserved host response, yet malarial sepsis exhibited a selective immunosuppressive signature (elevated IL-10, LILRB1, KIR3DL1, LAG3, TIM-4). A classifier comprising these proteins achieved AUCs of 0.73 and 0.72 with good calibration for identifying malarial sepsis.

Impact: This multicenter prospective analysis defines pathogen-associated immunologic heterogeneity in a high-burden setting and provides a validated protein signature for malarial sepsis stratification.

Clinical Implications: The immunosuppressive signature in malarial sepsis may guide future pathogen-stratified immunomodulatory trials and inform triage or risk enrichment strategies in endemic settings.

Key Findings

  • Malarial sepsis accounted for 20% and 28% of cases in discovery and validation cohorts, respectively.
  • ≤8% of proteins were differentially expressed between malarial and non-malarial sepsis after adjustment, indicating a largely conserved host response.
  • Malarial sepsis showed higher levels of immunosuppressive/exhaustion markers (e.g., IL-10, LILRB1, KIR3DL1, LAG3, TIM-4).
  • A proteomic classifier discriminated malarial sepsis with AUC 0.73 (0.65-0.81) and 0.72 (0.65-0.79), with Brier scores 0.14 and 0.18.

Methodological Strengths

  • Prospective multicenter design with separate discovery and validation cohorts
  • High-dimensional proteomic profiling with adjusted analyses for key confounders and external validation with calibration metrics

Limitations

  • Generalizability beyond Ugandan public hospitals may be limited
  • Observational design precludes causal inference and does not test targeted therapies

Future Directions: Test immunomodulatory strategies guided by the malarial immunosuppression signature and evaluate portability of the classifier across regions and assay platforms.

2. Metabolomics- and proteomics-based multi-omics integration reveals early metabolite alterations in sepsis-associated acute kidney injury.

73Level IIICohortBMC medicine · 2025PMID: 39934788

Integrating renal proteomics and metabolomics in LPS-induced mice highlighted five core metabolites, with time-resolved serum changes detected as early as 8 hours. A three-metabolite serum model (IC3: inosine, creatine, 3-hydroxybutyrate) discriminated SA-AKI from sepsis without AKI in 56 patients with an AUC of 0.90.

Impact: This study bridges mechanistic mouse data and human serum metabolomics to deliver an early diagnostic panel for SA-AKI with high discriminative performance.

Clinical Implications: If validated in broader populations, the IC3 panel could enable early SA-AKI detection and timely renoprotective strategies in sepsis care.

Key Findings

  • Identified 13 differential renal metabolites and 112 proteins in LPS-induced SA-AKI mice.
  • Five core metabolites (3-hydroxybutyric acid, 3-hydroxymethylglutaric acid, creatine, myristic acid, inosine) were linked to renal function and proteomic changes.
  • Serum myristic acid increased at 8 h; inosine decreased at 8 h; 3-hydroxybutyrate, 3-hydroxymethylglutaric acid, and creatine rose at 24 h in mice.
  • In a 56-patient clinical cohort, the IC3 model (inosine, creatine, 3-hydroxybutyrate) achieved AUC 0.90 for early SA-AKI identification.

Methodological Strengths

  • Multi-omics integration (renal proteomics and metabolomics) with time-resolved validation in vivo
  • Translational validation in a human clinical cohort with a parsimonious logistic model

Limitations

  • Clinical validation cohort was small (n=56) and from a single setting
  • External validation and assessment against standard biomarkers (e.g., NGAL, KIM-1) were not reported

Future Directions: Prospective multicenter validation, head-to-head comparison with established AKI biomarkers, and clinical utility assessments for early intervention.

3. Performance Evaluation of Prehospital Sepsis Prediction Models.

68.5Level IIICase-controlCritical care medicine · 2025PMID: 39937065

In a nested case-control study across four EDs, only PRESEP outperformed unaided EMS infection assessment and qSOFA for predicting which ambulance-transported adults would meet ED Sepsis-3 criteria, with AUPRC 0.33 versus 0.17 for unaided EMS. PRESEP’s sensitivity was 60% with a positive predictive value of 20%.

Impact: This study provides the first broad, head-to-head prehospital comparison showing that most models underperform, highlighting PRESEP as a pragmatic choice and underscoring the need for better EMS-targeted tools.

Clinical Implications: EMS systems may consider implementing PRESEP while developing or validating improved models, with attention to modest PPV and operational integration.

Key Findings

  • Among 21 prehospital sepsis models, only PRESEP outperformed unaided EMS assessment (AUPRC 0.33 vs 0.17; p < 0.001).
  • PRESEP also outperformed qSOFA (AUPRC 0.13; p < 0.001).
  • PRESEP showed 60% sensitivity and 20% positive predictive value among dichotomous predictors.

Methodological Strengths

  • Nested case-control design with rigorous model discrimination using AUPRC appropriate for imbalanced outcomes
  • Direct head-to-head evaluation of 21 models against real-world EMS assessment

Limitations

  • Single-state (Utah) data may limit generalizability to other EMS systems
  • Retrospective use of prospectively collected records; not an interventional deployment study

Future Directions: Prospective EMS implementation trials of PRESEP, model recalibration/augmentation with vital signs and biomarkers, and external validation across diverse EMS systems.