Educational resource · Not a medical device · Infectious diseases review in progress · Does not replace clinical judgement

Diagram — Endotoxin (LPS): from recognition to shock — SeptiMap

follow Gram-negative LPS from recognition (LBP, CD14, TLR4) to cytokines, then to coagulation and vasodilation. Educational resource, not a medical device.

Diagrams: mechanisms and principles

17 sourced diagrams · for medical students and practice

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Preclinical · clinical years

Endotoxin (LPS): from recognition to shock

Objective: follow Gram-negative LPS from recognition (LBP, CD14, TLR4) to cytokines, then to coagulation and vasodilation.

Step 5 / 5
Endotoxin (LPS): from recognition to shock1. LPS — Lipopolysaccharide is a component of the Gram-negative outer membrane; lipid A carries its toxicity. 2. Recognition — LBP transfers LPS to CD14, which presents it to the TLR4/MD-2 complex. 3. Signal and cytokines — Via MyD88 then NF-κB, the cell produces TNF-α, IL-1β and IL-6. 4. Coagulation — Tissue factor expression activates coagulation and can lead to DIC. 5. Vasodilation — Inducible NO synthase produces NO: vasodilation and hypotension.LPS (lipid A)outer membraneLBPCD14TLR4/MD-2MacrophageMyD88 → NF-κBTNF-α · IL-1β · IL-6Tissue factor→ coagulation→ DICiNOS → NO→ vasodilation→ hypotension
  • Pathogen
  • Toxin, damage
  • Host (cells, tissues)
  • Immunity
  • Clinical consequence

Key points

  • LPS: Gram-negative outer membrane component, toxicity carried by lipid A.
  • LBP → CD14 → TLR4/MD-2 → MyD88 → NF-κB → TNF-α, IL-1β, IL-6.
  • Tissue factor → DIC; NO → vasodilation and hypotension.

Classic pitfall

Treating LPS as a secreted toxin: it is a wall component, and the damage comes from the host response.

Related pathogen pages (8)

Sources

Educational content · Illustrative mechanisms · Not applicable to individual clinical decisions · MDR 2017/745

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