LL-37 exerts both direct and indirect antimicrobial effects. Its amphipathic, cationic α-helical structure (net +6 charge) allows it to preferentially bind and disrupt negatively charged microbial membranes[2]. Beyond direct killing, LL-37 modulates host immunity: in murine sepsis models, it induced neutrophils to release microvesicles rich in antimicrobial proteins, lowering bacterial burden and improving survival[3]. LL-37 can also bind bacterial lipopolysaccharide (LPS) and block its interaction with CD14/TLR4, reducing endotoxin-triggered TNF release and neutrophil apoptosis[2]. These combined mechanisms help explain its potential in infection control and tissue-repair contexts.