Inflammatory response in bacteremia survivors and non-survivors: a case-control study

Abstract

Abstract Survival in bacteremia is influenced by host comorbidities, pathogen virulence, immune response, and the quality of medical care. A deeper understanding of host inflammatory responses may help identify new biomarkers and therapeutic targets to improve outcomes. In this study, we analyzed plasma samples from adult patients with bacteremia who presented to the emergency department. Patients who died within seven days ( n  = 44) were compared to matched survivors ( n  = 44) who lived at least 90 days, with matching based on age, sex, and causative bacterium. Relative concentrations of 92 inflammation-related plasma proteins were measured using the proximity extension assay (Olink Proteomics AB). Of these, 82 proteins were successfully quantified. Thirty proteins, including IL-20RA, CD40, and HGF, were significantly elevated in non-survivors, while three proteins—IFNG, Flt3L, and TNFB—were significantly reduced. Pathway enrichment analysis revealed activation of multiple proinflammatory signaling cascades in non-survivors, particularly those involving IL-6, IL-23, and IL-17. Logistic regression identified HGF, IL-17 C, and Flt3L as key discriminative proteins between groups. These findings indicate that the host inflammatory profile in bacteremia differs markedly between survivors and early non-survivors. Our results highlight potential diagnostic biomarkers for identifying high-risk patients and point to promising therapeutic targets in the management of bacteremia.