Human antimicrobial/host defense peptide LL-37 may prevent the spread of a local infection through multiple mechanisms: an update

被引:1
作者
Svensson, Daniel [1 ]
Nilsson, Bengt-Olof [1 ]
机构
[1] Lund Univ, Dept Expt Med Sci, BMC D12, S-22184 Lund, Sweden
关键词
Antimicrobial peptides (AMPs); Apoptosis; Cathelicidin/LL-37; Host cell cytotoxicity; Infection; Inflammation; HUMAN CATHELICIDIN LL-37; GINGIVAL CREVICULAR FLUID; RECEPTOR-LIKE; HUMAN MACROPHAGES; IMMUNE-RESPONSES; HUMAN CAP18; APOPTOSIS; ACTIVATION; CELLS; INFLAMMASOME;
D O I
10.1007/s00011-025-02005-8
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
BackgroundHuman cathelicidin LL-37 shows activity towards both gram-positive and gram-negative bacteria, and it is also active against some types of viruses. Besides its antimicrobial effects, the peptide modulates innate immunity through binding and inactivation of bacterial endotoxins and promoting chemotaxis of immune cells.ResultsLL-37 is reported to interact with plasma membrane receptors and mediate import of Ca2+. Importantly, LL-37 has both anti- and pro-inflammatory effects. LL-37 is cytotoxic to many different human cell types, particularly infected cells, when administered to the cells at final concentrations of 1-10 mu M. In psoriatic lesions very high concentrations (300 mu M) of the peptide are detected, and in periodontitis, gingival crevicular fluid contains about 1 mu M LL-37, implying high concentrations of the peptide at the site of infection/inflammation which can affect host cell viability locally.ConclusionsAltogether, LL-37 may inhibit and prevent the infection from spreading by direct anti-bacterial and anti-viral effects, but also via anti- and pro-inflammatory mechanisms, and through killing already infected and weakened host cells at the site of infection/inflammation.
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页数:10
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