LL-37
A human cathelicidin antimicrobial peptide central to skin and respiratory innate immunity.
In plain English
LL-37 is the only human cathelicidin antimicrobial peptide. It is produced by neutrophils, epithelial cells, and skin keratinocytes, where it kills bacteria, fungi, and some viruses, and shapes inflammation and wound healing. LL-37 levels relate to vitamin D status and to disease severity in several skin and respiratory conditions. As a therapeutic, LL-37 has been investigated for diabetic foot ulcers, wound healing, and select infections, but no LL-37-based drug is currently FDA-approved. People commonly research LL-37 for immune support and wound healing, but the human therapeutic dataset is limited.
What it is
LL-37 is a 37-amino-acid cationic antimicrobial peptide derived from cleavage of the human cathelicidin precursor hCAP-18 by proteases such as proteinase 3 and kallikreins.
Mechanism (summary)
LL-37 disrupts microbial membranes, neutralizes bacterial endotoxin, modulates chemotaxis of immune cells, supports angiogenesis, and acts as a key effector of vitamin-D-driven innate immunity.
Why people research it
- Diabetic foot ulcers and wound healing
- Respiratory innate immunity
- Antimicrobial resistance and infection
- Skin barrier conditions including atopic dermatitis and rosacea
Human evidence
Early-phase trials of topical LL-37 in diabetic foot ulcers have shown improved healing rates. Observational studies link LL-37 levels to outcomes in respiratory infection and skin disease. Large RCTs of LL-37 as a drug are limited.
Animal / lab evidence
Robust antimicrobial and immunomodulatory activity in animal infection and wound-healing models.
Key studies
Each summary explains the design, what was found, and what it doesn't prove.
In a small trial, topical LL-37 helped leg ulcers heal better than placebo.
Vitamin D made human immune cells produce more LL-37, which helped them kill TB bacteria in a dish.
History
LL-37 was identified in the 1990s as the human cathelicidin antimicrobial peptide and has been central to innate-immunity research since.
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