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LPS Endotoxaemia vs CLP Polymicrobial Sepsis
Two primary models serve different research questions. LPS endotoxaemia (E. coli LPS 10–15 mg/kg i.p. in C57BL/6J) is preferred for mechanistic studies of the TLR4-NF-κB cytokine storm, gut barrier biology, and microvascular dysfunction — it provides a control
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- Two primary models serve different research questions. LPS endotoxaemia (E. coli LPS 10–15 mg/kg i.p. in C57BL/6J) is preferred for mechanistic studies of the TLR4-NF-κB cytokine storm, gut barrier biology, and microvascular dysfunction — it provides a controlled, reproducible LPS dose with predictable peak cytokine kinetics (TNF-α peak at 90 min, IL-6 peak at 3h, HMGB1 peak at 16–24h). CLP (18-gauge needle, 3 cm poke, 1 faecal extrusion — inducing peritonitis and polymicrobial bacteraemia) is preferred for immune response biology, survival endpoints, and secondary infection resistance studies — because CLP produces living bacteria rather than purified endotoxin and better models the immunosuppressive phase. Critical design requirement: for survival studies, antibiotic (imipenem 25 mg/kg i.m. at 6 and 12 hours post-CLP) with or without fluid resuscitation must be specified, as un-resuscitated CLP produces 70–90% mortality without antibiotic, which may be too high for demonstrating a su