Understand the source comparison
LL-37 for Gut Health Research Evidence: Comparison
DSS-induced colitis (mouse) Barrier protection + anti-inflammatory 48% reduction in disease activity index; 62% decrease in myeloperoxidase activity 5 mg/kg IP daily × 7 days Strongest evidence for barrier repair. Mechanism translates to human pathophysiology
No winner is assigned.
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- DSS-induced colitis (mouse)
- Barrier protection + anti-inflammatory
- 48% reduction in disease activity index; 62% decrease in myeloperoxidase activity
- 5 mg/kg IP daily × 7 days
- Strongest evidence for barrier repair. Mechanism translates to human pathophysiology
- LL-37 knockout mice (colitis)
- Loss-of-function model
- 65% mortality vs 22% in wild-type; increased bacterial translocation and ulceration
- N/A (genetic model)
- Demonstrates causal role rather than correlation. Critical for understanding endogenous function
- C. difficile infection (mouse)
- Antimicrobial selectivity
- 72% reduction in pathogen load; commensal populations preserved
- 10 mg/kg IP
- Selective pathogen targeting without dysbiosis. Major advantage over antibiotics
- Ulcerative colitis (human pilot)
- Topical mucosal delivery
- Mean 1.8-point improvement in endoscopic Mayo score; 4.1-fold LL-37 expression increase
- Topical enema (14 days)
- Early-phase evidence only. Requires larger RCT for clinical validation
- SIBO model (rat)
- Oral administration + bacterial overgrowth
- 58% reduction in jejunal bacterial counts; normalized D-lactate
- Oral (encapsulated) × 10 days
- Demonstrates oral feasibility. Critical for non-invasive delivery
- Serial passage resistance (in vitro)
- Resistance development potential
- No MIC increase after 30 passages (E. coli)
- Sublethal exposure
- Membrane disruption mechanism prevents traditional resistance. Unique among antimicrobials