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抗菌肽LL-37可抑制HIV-1复制。

The antimicrobial peptide LL-37 inhibits HIV-1 replication.

作者信息

Bergman Peter, Walter-Jallow Lilian, Broliden Kristina, Agerberth Birgitta, Söderlund Johan

机构信息

Department of Medicine, Centre for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Solna, Stockholm, Sweden.

出版信息

Curr HIV Res. 2007 Jul;5(4):410-5. doi: 10.2174/157016207781023947.

Abstract

The antimicrobial peptide LL-37 is the only cathelicidin that has been described in humans. LL-37 exerts chemotactic, immunomodulatory and angiogenic effects; activities that are mediated through binding to the formyl peptide receptor like (FPRL)-1 receptor. Agonistic ligation of FPRL-1 can also induce down-regulation of HIV-1 chemokine receptors and reduce susceptibility to HIV-1 infection in vitro. Therefore, we have evaluated the capacity of LL-37 to inhibit HIV-1 infection in vitro. Here we demonstrate that LL-37 inhibits HIV-1 replication in PBMC, including primary CD4(+) T cells. This inhibition was readily reproduced using various HIV-1 isolates without detectable changes in the target cell expression of HIV-1 chemokine receptors. Accordingly, the HIV-1 inhibitory effect was shown to be independent of FPRL-1 signalling. Given the epithelial expression of LL-37, it may contribute to the local protection against HIV-1 infection.

摘要

抗菌肽LL-37是人类中已被描述的唯一一种cathelicidin。LL-37具有趋化、免疫调节和血管生成作用;这些活性是通过与类甲酰肽受体(FPRL)-1受体结合介导的。FPRL-1的激动性连接还可诱导HIV-1趋化因子受体的下调,并在体外降低对HIV-1感染的易感性。因此,我们评估了LL-37在体外抑制HIV-1感染的能力。在此我们证明LL-37可抑制PBMC(包括原代CD4(+) T细胞)中的HIV-1复制。使用各种HIV-1分离株均可轻易重现这种抑制作用,而HIV-1趋化因子受体的靶细胞表达未检测到变化。因此,HIV-1抑制作用显示独立于FPRL-1信号传导。鉴于LL-37的上皮表达,它可能有助于局部抵抗HIV-1感染。

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