Abstract

Over the past two decades, elucidation of the host response to severe infection has uncovered the complex and dynamic derangements in immune, endothelial, and metabolic homeostasis that underlie sepsis pathobiology.1,2 Leveraging advances in high-dimensional host response profiling and computational methods (e.g., machine learning, structural equation modelling), identification of patient subgroups defined by distinct clinico-molecular features (“subphenotypes”) and pathobiological mechanisms (“endotypes”) represents a promising approach to achieve biological deconvolution of the heterogenous sepsis phenotype.

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