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Antimicrobial Peptides advanced

LL-37

LL-37 is the only human cathelicidin antimicrobial peptide, derived from hCAP18, with broad-spectrum activity against bacteria, viruses, and fungi plus immunomodulatory functions.

By Encyclopeptide Editorial | 3 min read
cathelicidin antimicrobial innate-immunity LL-37 hCAP18

Chemical Identity

PropertyValue
Chemical FormulaC205H340N60O53
Molecular Weight4493.36 g/mol
CAS Number154947-66-7
IUPAC NameCathelicidin antimicrobial peptide
Peptide ClassCathelicidin
Sequence HomologyC-terminal fragment of human hCAP18

Structure

LL-37 is a 37-amino acid amphipathic, cationic alpha-helical peptide. Its name derives from the N-terminal residues (two leucines) and total length. LL-37 is cleaved from the 18 kDa precursor hCAP18 (human cationic antimicrobial protein 18) by proteinase 3 and other serine proteases. The peptide contains six positively charged residues (lysine and arginine) distributed along one face of the amphipathic helix, with hydrophobic residues on the opposite face.

Mechanism of Action

LL-37 disrupts microbial membranes through a carpet-like mechanism:

  1. Membrane binding: Cationic residues interact with negatively charged bacterial membrane phospholipids (phosphatidylglycerol, cardiolipin)
  2. Helix insertion: The amphipathic helix inserts parallel to the membrane surface
  3. Membrane disruption: Above a threshold concentration, the peptide forms toroidal pores, causing membrane permeabilization and cell lysis

Beyond direct killing, LL-37 has potent immunomodulatory functions including chemotaxis of neutrophils and monocytes, promotion of wound healing, and modulation of cytokine responses.

Biological Functions

LL-37 is expressed by epithelial cells, neutrophils, macrophages, and mast cells. It is present in sweat, saliva, airway surface liquid, and wound fluid. Key roles include:

  • Antimicrobial defense: Active against gram-positive and gram-negative bacteria, enveloped viruses, and fungi
  • Wound healing: Promotes keratinocyte migration and re-epithelialization
  • Immune modulation: Neutralizes LPS, modulates dendritic cell differentiation
  • Anti-biofilm: Prevents biofilm formation and disrupts established biofilms

Clinical Relevance

LL-37 expression is reduced in atopic dermatitis, chronic wounds, and cystic fibrosis. Psoriasis patients have elevated LL-37 levels, which paradoxically may drive autoimmune inflammation through LL-37-DNA complexes that activate plasmacytoid dendritic cells. Therapeutic applications under investigation include wound healing formulations, anti-infective coatings, and cancer immunotherapy.

Safety and Side Effects

At physiological concentrations, LL-37 is well-tolerated. High concentrations can cause cytotoxicity to host cells, hemolysis, and pro-inflammatory responses. The therapeutic window between antimicrobial and cytotoxic concentrations is being studied for clinical applications.

References

  • Gudmundsson, G.H., et al. (1996). The human gene FALL39 and processing of the cathelin precursor to the antibacterial peptide LL-37 in granulocytes. European Journal of Biochemistry, 238, 325-332.
  • Vandamme, D., et al. (2012). A comprehensive summary of LL-37, the factotum human cathelicidin peptide. Cellular Immunology, 280, 22-35.

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