LL-37 contains 37 amino acid residues with the first two leucine residues (L1LGDFFRKSKEKIGKEFKRIVQRIKDFLRNLVPRTES37) and mostly exists in epithelial cells and neutrophils.
In vitro experiment it shown that treatment with 4 and 10 μM LL-37 reduced both the number and viability of human osteoblast-like MG63 cell.[2] In vitro, the pretreatment of pMSCs with 1 and 10 μg/mL of LL-37 had not effect on the migratory cells ability. But the pretreatment with 1 μg/mL of LL-37 increased the migratory potential of pMSCs after 48 h.[4] In vitro study it indicated that at 1 μmol/L concentrations of LL-37 for 24 hours, LL-37 prevented LPS-induced stimulation of MCP-1 expression analyzed both on transcript and on protein levels, but had no effect on toll-like receptor (TLR)2 and TLR4 transcript expression. In the meanwhile, treatment with 0.1 and 1 μmol/L LL-37 for 60 minutes in PDL cell induced immunoreactivity for LL-37.[5]
In vivo study it suggested that treatment with 2 μg/mouse of LL-37 intravenously improves the survival of CLP septic mice in a dose-dependent effect. LL-37 ameliorates the level of ectosomes with higher antibacterial potential, result in reducing the bacterial load in CLP mice.[1] LL-37 dose-dependently (1, 3, or 10 μg/ml) induced ectosome release from neutrophil. Injection LL-37 supressed the infiltration of polymorphonuclear cells in CLP mice, where the bacterial burden and inflammatory response are decreased.[3]
References:
[1].Nagaoka I, et al. Therapeutic Potential of Cathelicidin Peptide LL-37, an Antimicrobial Agent, in a Murine Sepsis Model. Int J Mol Sci. 2020 Aug 19;21(17):5973.
[2].Bankell E, et al. LL-37-induced caspase-independent apoptosis is associated with plasma membrane permeabilization in human osteoblast-like cells. Peptides. 2021 Jan;135:170432.
[3].Kumagai Y, et al. Antimicrobial peptide LL-37 ameliorates a murine sepsis model via the induction of microvesicle release from neutrophils. Innate Immun. 2020 Oct;26(7):565-579.
[4].Oliveira-Bravo M, et al. LL-37 boosts immunosuppressive function of placenta-derived mesenchymal stromal cells. Stem Cell Res Ther. 2016 Dec 30;7(1):189.
[5].Aidoukovitch A, et al. The host defense peptide LL-37 is internalized by human periodontal ligament cells and prevents LPS-induced MCP-1 production. J Periodontal Res. 2019 Dec;54(6):662-670.
LL-37含有37个氨基酸残基,前两个亮氨酸残基（L1LGDFFRKSKEKIGKEFKRIVQRIKDFLRNLVPRTES37）,主要存在于上皮细胞和中性粒细胞中。
体外实验表明,用 4 μM 和 10 μM LL-37 处理会降低人成骨细胞样 MG63 细胞的数量和活力。[2] 在体外,用1和10μg/mL的LL-37对迁移细胞能力没有影响。但用1 μg/mL LL-37预处理48 h后pMSCs的迁移潜能增加。[4] 体外研究表明,在1 μmol/L浓度的LL-37下处理24小时,LL-37 阻止了 LPS 诱导的 MCP-1 表达刺激,在转录本和蛋白质水平上进行了分析,但对 Toll 样受体 (TLR)2 和 TLR4 转录本表达没有影响。同时,0.1 和 1 μmol/L LL-37 在 PDL 细胞中处理 60 分钟可诱导 LL-37 的免疫反应。[5]
体内研究表明,每只小鼠静脉注射 2 μg LL-37 可提高 CLP 脓毒症小鼠的存活率,并具有剂量依赖性效应。 LL-37 改善具有更高抗菌潜力的胞外体水平,从而减少 CLP 小鼠的细菌负荷。[1] LL-37 剂量依赖性（1、3 或 10 μg/ml）诱导中性粒细胞胞外体释放。注射 LL-37 抑制了 CLP 小鼠体内多形核细胞的浸润,从而降低了细菌负荷和炎症反应。[3]