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首页> 外文期刊>Cellular immunology >Effect of the antimicrobial peptide LL-37 on Toll-like receptors 2-, 3- and 4-triggered expression of IL-6, IL-8 and CXCL10 in human gingival fibroblasts.
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Effect of the antimicrobial peptide LL-37 on Toll-like receptors 2-, 3- and 4-triggered expression of IL-6, IL-8 and CXCL10 in human gingival fibroblasts.

机译：抗菌肽LL-37对Toll样受体2、3和4触发的人牙龈成纤维细胞IL-6，IL-8和CXCL10表达的影响。

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摘要

The antimicrobial peptide LL-37 is known to have a potent LPS-neutralizing activity in monocytes and macrophages. Recently, LL-37 in gingival crevicular fluids is suggested to be the major protective factor preventing infection of periodontogenic pathogens. In this study, we tried to address the effect of LL-37 on proinflammatory responses of human gingival fibroblasts (HGFs) stimulated with Toll-like receptor (TLR)-stimulant microbial compounds. LL-37 potently suppressed LPS-induced gene expression of IL6, IL8 and CXCL10 and intracellular signaling events, degradation of IRAK-1 and IkappaBalpha and phosphorylation of p38 MAPK and IRF3, indicating that the LPS-neutralizing activity is also exerted in HGFs. LL-37 also suppressed the expression of IL6, IL8 and CXCL10 induced by the TLR3 ligand poly(I:C). LL-37 modestly attenuated the expression of IL6 and IL8 induced by the TLR2/TLR1 ligand Pam(3)CSK(4), but did not affect the expression induced by the TLR2/TLR6 ligand MALP-2. Interestingly, LL-37 rather upregulated the expression of IL6, IL8 and CXCL10 induced by another TLR2/TLR6 ligand FSL-1. Thus, the regulatory effect of LL-37 is differently exerted towards proinflammatory responses of HGFs induced by different microbial stimuli, which may lead to unbalanced proinflammatory responses of the gingival tissue to infection of oral microbes.
机译：已知抗菌肽LL-37在单核细胞和巨噬细胞中具有有效的LPS中和活性。最近，牙龈沟液中的LL-37被认为是预防牙周病原体感染的主要保护因素。在这项研究中，我们试图解决LL-37对用Toll样受体（TLR）刺激性微生物化合物刺激的人牙龈成纤维细胞（HGF）促炎反应的作用。 LL-37有效抑制LPS诱导的IL6，IL8和CXCL10的基因表达以及细胞内信号转导事件，IRAK-1和IkappaBalpha的降解以及p38 MAPK和IRF3的磷酸化，表明LGF中和活性也发挥在HGF中。 LL-37还抑制了TLR3配体poly（I：C）诱导的IL6，IL8和CXCL10的表达。 LL-37适度减弱了TLR2 / TLR1配体Pam（3）CSK（4）诱导的IL6和IL8的表达，但没有影响TLR2 / TLR6配体MALP-2诱导的表达。有趣的是，LL-37上调了另一种TLR2 / TLR6配体FSL-1诱导的IL6，IL8和CXCL10的表达。因此，LL-37的调节作用不同地作用于由不同微生物刺激诱导的HGF的促炎反应，这可能导致牙龈组织对口腔微生物感染的促炎反应不平衡。

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