sepsis
Definition
Sepsis is a life-threatening systemic inflammatory response syndrome (SIRS) caused by dysregulated host immune responses to infection. It occurs when the body's response to pathogens triggers widespread inflammation, leading to tissue damage, organ dysfunction, and potentially septic shock. Sepsis involves complex interactions between pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs), and immune signaling cascades including cytokine storms. Key mediators include TNF-α, IL-1β, IL-6, and complement activation. The condition progresses through stages from infection to sepsis, severe sepsis, and septic shock, with mortality rates increasing at each stage. Understanding sepsis pathophysiology requires mapping intricate networks of immune cells, inflammatory mediators, coagulation factors, and endothelial dysfunction that collectively determine patient outcomes.
Visualize sepsis in Nodes Bio
Researchers can use Nodes Bio to map sepsis pathophysiology networks, visualizing interactions between immune cells, cytokines, complement proteins, and coagulation factors. Network analysis reveals critical regulatory nodes in inflammatory cascades, identifies potential therapeutic targets, and models how interventions might modulate dysregulated immune responses. Causal inference tools help distinguish protective versus pathological immune pathways in sepsis progression.
Visualization Ideas:
- Cytokine-immune cell interaction networks showing inflammatory cascade progression
- Host-pathogen interaction maps linking PAMPs to immune receptor signaling pathways
- Multi-omics integration networks combining transcriptomics, proteomics, and clinical outcomes in sepsis patients
Example Use Case
A pharmaceutical team investigating sepsis therapeutics uses network visualization to map the cytokine storm cascade. They integrate transcriptomic data from septic patient samples with known protein-protein interactions, revealing that IL-6 trans-signaling acts as a central hub connecting multiple inflammatory pathways. By overlaying drug target data, they identify JAK-STAT pathway inhibitors as promising candidates. The network analysis shows these compounds could dampen inflammation without completely suppressing protective immunity, leading to prioritization of three candidates for preclinical testing in sepsis models.