Antimicrobial peptide inhibition of Porphyromonas gingivalis 381-induced hemagglutination is improved with a synthetic decapeptide

Antimicrobial peptide inhibition of Porphyromonas gingivalis 381-induced hemagglutination is improved with a synthetic decapeptide
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DOI:
10.1016/j.peptides.2009.07.027
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发表时间:
2009-12-01
期刊:
影响因子:
3
通讯作者:
Leung, Kai P.
Leung, Kai P.
中科院分区:
医学3区
文献类型:
--
作者:
Dixon, Douglas R.;Jeffrey, Nicole R.;Leung, Kai P.

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研究了各种抗菌肽(AMP)对口腔致病菌牙龈卟啉单胞菌(Porphyromonas gingivalis)细胞成分血凝能力的影响。使用囊泡(VES)或外膜(OM)制剂,在标准化血凝试验中使用各种哺乳动物红细胞测定了AMP对牙龈卟啉单胞菌381诱导的血凝的抑制作用。合成的十肽(KSL-W)及其截短的肽类似物进行了评估,并与选定的类别的AMP来自天然存在的先天防御肽进行了比较。除了爪蟾抗菌肽I和截短的KSL-W类似物之外,所有测试的AMP都有效地破坏测试的红细胞中牙龈卟啉单胞菌诱导的血凝。LL-37通常是最有效的,其次是组胺素5。发现合成的十肽(KSL-W)在抑制作用方面与组胺素8肽相似。此外,采用联合应用试验(使用选定的口服相关AMP +/- KSL-W)来确定联合应用程序是否会改善血凝消除,使其高于单独口服相关AMP。这些实验表明,KSL-W肽改善的血凝抑制作用高于每种口服相关肽(组胺抑制素5和8)。LL-37)单独。在哺乳动物红细胞中,对于凯萨林菌素类AMP、LL-37和indolicidin(分别>= 25和>= 100 μ M)观察到显著的肽诱导的血凝。相反,KSL-W在所有试验浓度范围内(0.1-1000 μ M)均不诱导红细胞凝集。我们的研究结果表明,几种AMP是有效的破坏牙龈卟啉单胞菌381诱导的血凝和共同应用的一个小的,合成衍生的肽可能有助于增强本地主机AMP参与先天防御的作用。爱思唯尔公司出版
The effects of various antimicrobial peptides (AMPs) on disrupting the hemagglutinating ability of cellular components of the putative oral pathogen Porphyromonas gingivalis were examined. AMP inhibition of A gingivalis 381-induced hemagglutination using vesicles (VES) or outer membrane (OM) preparations was determined within standardized hemagglutination assays using various mammalian erythrocytes. A synthetic decapeptide (KSL-W) and its truncated peptide analogs were evaluated and compared with selected classes of AMPs derived from naturally occurring innate defense peptides. All tested AMPs were effective in disrupting A gingivalis-induced hemagglutination among tested erythrocytes, with the exception of magainin I and the truncated KSL-W analogs. LL-37 was generally the most potent followed by histatin 5. The synthetic decapeptide (KSL-W)was found to be similar to the histatin 8 peptide in terms of inhibitory effect. In addition, co-application assays (with selected oral-related AMPs +/- KSL-W) were employed to determine if co-application procedures would improve hemagglutination abrogation above that of oral-related AMPs alone. These experiments revealed that the KSL-W peptide improved hemagglutination inhibition above that of each of the oral-related peptides (histatin 5 and 8. LL-37) alone. Among mammalian erythrocytes, significant peptide-induced hemagglutination was observed for the cathelicidin class AMPs, LL-37 and indolicidin (>= 25 and >= 100 mu M respectively). In contrast, KSL-W did not induce erythrocyte agglutination throughout any concentration range tested (0.1-1000 mu M). Our results suggest that several AMPs are effective in disrupting A gingivalis 381-induced hemagglutination and that the co-application of a small, synthetically derived peptide may serve to augment the role of local host AMPs engaged in innate defense. Published by Elsevier Inc.