Understand the source comparison
LL-37 Results After 1 Month: Mechanism Comparison
Direct antimicrobial activity 6–48 hours CFU reduction of 90–99% in bacterial cultures; fungal growth inhibition CFU plating, MIC assays This is the fastest LL-37 mechanism. Membrane disruption is immediate and doesn't require downstream signalling Pro-inflamm
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- Direct antimicrobial activity
- 6–48 hours
- CFU reduction of 90–99% in bacterial cultures; fungal growth inhibition
- CFU plating, MIC assays
- This is the fastest LL-37 mechanism. Membrane disruption is immediate and doesn't require downstream signalling
- Pro-inflammatory cytokine suppression
- 7–12 days
- IL-6 reduced by 40–60%; TNF-alpha reduced by 30–50% vs baseline
- ELISA, multiplex cytokine panels
- Cytokine reductions stabilise by week 3. Earlier measurements may miss the full effect
- Wound closure and re-epithelialisation
- 14–28 days
- 50–60% faster wound closure in impaired healing models; increased keratinocyte migration
- Planimetry, histological sectioning
- Visible tissue changes lag behind biochemical shifts. This is a structural remodeling process, not just inflammation control
- Regulatory T-cell expansion
- 20–35% increase in CD4+CD25+FoxP3+ Treg frequency
- Flow cytometry
- Treg expansion is one of the slowest LL-37 effects but may be the most durable. Systemic immune balance shifts require sustained signalling
- Chemotaxis and immune cell recruitment
- 3–10 days
- Peak neutrophil and monocyte infiltration at infection/injury sites
- Immunohistochemistry, cell tracking
- Immune cell recruitment happens before visible healing. This is the bridge between immediate antimicrobial action and delayed tissue repair