LL-37
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LL-37 Provides Immune Defense Against Bacterial, Viral and Fungal Invasion.
LL-37 disrupts the lipid bilayer without breaking the membrane into small fragments, and fluorescence measurements also suggested a pore forming mechanism. The activity against mammalian cell membranes is also ambiguous: it was proposed that LL-37 could act, at least in part, by decreasing the fluidity and hence lowering the permeability of epithelial cell membranes, making it harder for certain bacteria to attack. Hence, there are many uncertainties around the mechanism of LL-37 action and attention has shifted to developing more active variants of LL-37 using systematic mutation while the study of the actual mechanism of action has been largely neglected.
LL-37 also has an indirect role in the immune response to foreign antigens. It displays an ability to activate various immune cells thus possessing functional dualism in the human body. Following stimulation by proinflammatory signals hCAP18 is released into the extracellular environment and cleaved by proteinase 3 in neutrophils and kallikrein. Exposure to LL-37 results in recruitment of inflammatory cells, induction of M1 macrophages, and stimulation of inflammatory responses such as inflammasome activation and type 1 IFN production. LL-37 has strong anti-inflammatory effects such as neutralization of TLR4 activation by LPS, downmodulation of inflammatory cytokine responses, and preventing invasion and inflammatory responses to pathogenic bacteria.
LL-37 blocks an enzyme required by the original coronavirus and may eliminate damaged cells without inflammation.
LL-37 selectively inhibits the Cathepsin L protease involved in SARS-CoV activation while partially enhancing proteases Cathepsins S and K.
LL-37 inhibits cathepsin L at a concentration of 150 nM. (15) Cathepsin L primes (helps activate) the SARS-CoV RNA virus when it is entering the cell. (16)