Antimicrobial peptide LL-37 attenuates LTA induced inflammatory effect in macrophages
Antimicrobial peptide LL-37 attenuates LTA induced inflammatory effect in macrophages
复制标题
抗菌肽 LL-37 减弱 LTA 诱导的巨噬细胞炎症作用
DOI：
10.1016/j.intimp.2013.01.012
复制
发表时间：
2013-03-01
影响因子：
5.6
通讯作者：
Sun, Tieying
中科院分区：
文献类型：
--
作者：
Ruan, Yang;Shen, Tao;Sun, Tieying
LL-37/hCAP-18作为唯一的人源性cathelicidin，在炎症反应中发挥重要作用。脂磷壁酸（Lipoteichoic add，LTA）是金黄色葡萄球菌（Staphylococcus aureus）的重要组成成分，是人类严重呼吸道感染的常见病原菌之一，近年来发病率不断上升。本研究旨在探讨LL-37在LTA诱导的巨噬细胞炎症反应中的作用。我们检测了LL-37处理后TNF-α和IL-6的产生，并讨论了其信号转导途径，如p38 MAPK和Akt激活巨噬细胞。实时荧光定量RT-PCR和酶联免疫吸附试验（ELISA）分析促炎细胞因子的表达。Western blot和免疫荧光染色检测LL-37的表达。结果表明，LL-37在LTA处理后上调。在一定浓度范围内，它能抑制LTA诱导的p38 MAPK和Ala磷酸化，并能抑制巨噬细胞产生TNF-α和IL-6。这些结果表明，LL-37发挥抗炎特性并减弱巨噬细胞中的促炎细胞因子释放。皇冠版权所有（C）2013由爱思唯尔B. V.出版保留所有权利。
LL-37/hCAP-18, as the only human cathelicidin, plays an important role in inflammation. Lipoteichoic add (LTA) is an important bacterial component of Staphylococcus aureus, which is one of the common human pathogens for severe respiratory infection with increasing morbidity in recent years. The present study is to investigate the role of LL-37 in LTA induced inflammatory reaction in macrophages. We examined TNF-alpha and IL-6 production after LL-37 treatment and discussed its signal transduction pathways such as p38MAPK and Akt activation in macrophages. The expression of pro-inflammatory cytokines was analyzed by quantitative real-time RT-PCR and enzyme-linked immunosorbent assay (ELISA). The LL-37 expression was determined by Western blot and immunofluorescence staining. The results showed that LL-37 was upregulated after LTA treatment. It could inhibit LTA induced p38MAPK and Ala phosphorylation and attenuate TNF-alpha and IL-6 production in macrophages in some specific concentration. These results suggest that LL-37 exerts an anti-inflammatory property and attenuates the pro-inflammatory cytokine release in macrophages. Crown Copyright (C) 2013 Published by Elsevier B.V. All rights reserved.