Human endogenous antibiotic LL-37 stimulates airway epithelial cell proliferation and wound closure.
Shaykhiev. Renat R; Beisswenger. Christoph C; Kändler. Kerstin K; Senske. Judith J; Püchner. Annette A; Damm. Thomas T; Behr. Jürgen J; Bals. Robert R
Key Findings
- LL‑37 promotes wound closure in airway epithelial cells at 1‑5 µg/ml
- The effect requires serum and involves EGFR, a G‑protein‑coupled receptor, and MAPK signaling
- LL‑37 stimulates both cell proliferation and migration in vitro
Practical Outcomes
- For now, there’s no direct protocol for taking LL‑37 to improve lung health. The results suggest that boosting your body’s own LL‑37 (e.g., via vitamin D) might support airway repair, but any supplementation would need clinical testing first.
Summary
The study shows that the natural human peptide LL‑37 can help airway cells grow and close wounds in lab dishes, working at low microgram‑per‑millilitre levels, but only when serum is present. It does this by activating growth‑related pathways like the epidermal growth factor receptor and MAPK. This is an early‑stage, cell‑culture finding, not a tested human treatment.
Abstract
Antimicrobial peptides are endogenous antibiotics that directly inactivate microorganisms and in addition have a variety of receptor-mediated functions. LL-37/hCAP-18 is the only cathelicidin found in humans and is involved in angiogenesis and regulation of the innate immune system. The aim of the present study was to characterize the role of the peptide LL-37 in the regulation of wound closure of the airway epithelium in the cell line NCI-H292 and primary airway epithelial cells. LL-37 stimulated healing of mechanically induced wounds in monolayers of the cell line and in differentiated primary airway epithelium. This effect was detectable at concentrations of 5 mug/ml in NCI-H292 and 1 mug/ml in primary cells. The effect of LL-37 on wound healing was dependent on the presence of serum. LL-37 induced cell proliferation and migration of NCI-H292 cells. Inhibitor studies in the wound closure and proliferation assays indicated that the effects caused by LL-37 are mediated through epidermal growth factor receptor, a G protein-coupled receptor, and MAP/extracellular regulated kinase. In conclusion, LL-37 induces wound healing, proliferation, and migration of airway epithelial cells. The peptide is likely involved in the regulation of tissue homeostasis in the airways.
Study Information
pubmed
2005
2005-06-17T00:00:00.000Z
10.1152/ajplung.00286.2004