Carbamylation makes LL-37 damage tissue

This proposed mechanism asks why an immune defence that kills bacteria might also injure the body’s own tissue. It focuses on LL-37, a human cathelicidin: a short antimicrobial peptide released by myeloid cells, immune cells that help fight infection. Cyanate in tissue could carbamylate LL-37 by attaching a chemical group to its amino end. The altered form is proposed to retain bacterial killing while increasing host-cell damage. The key test holds peptide secretion and early infection burden equal, then asks whether damage follows the fraction of altered LL-37. Defined peptide variants and targeted mass spectrometry, which identifies molecular forms and modification sites, could test this in human cell and tissue models.