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金葡菌选择性诱导角质形成细胞产生抗菌肽。

Selective induction of antimicrobial peptides from keratinocytes by staphylococcal bacteria.

机构信息

Department of Dermatology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

出版信息

Microb Pathog. 2013 Mar;56:35-9. doi: 10.1016/j.micpath.2012.11.005. Epub 2012 Nov 20.

DOI:10.1016/j.micpath.2012.11.005
PMID:23178253
Abstract

Staphylococcus aureus (S. aureus) is one of the most clinically important inflammation-inducing pathogens, while Staphylococcus epidermidis (S. epidermidis) is nonpathogenic and hardly causes inflammation on skin. β-defensins, antimicrobial peptides, are secreted from keratinocytes constitutively or upon induction by various microorganisms. However, the difference between S. aureus and S. epidermidis is still unclear in terms of their influences on the production of β-defensins. In this study, we focused on the influences of S. aureus and S. epidermidis on the keratinocyte innate immune response. Pathogenic S. aureus mainly induced human β-defensin (hBD) 1 and hBD3, but not hBD2, and nonpathogenic S. epidermidis mainly induced hBD2 from human keratinocytes. Molecular weight fractions of >10 kDa prepared from S. aureus supernatants induced the production of hBD1 and hBD3. On the other hand, molecular weight fraction of >100 kDa prepared from S. epidermidis supernatants induced the production of hBD2.Furthermore, the secreted products of S. epidermidis used the toll-like receptor (TLR) 2 pathway in the induction of hBD2 production. The secreted products of S. aureus and S. epidermidis differentially induced subtypes of hBD through different receptors, which may be associated with the difference in virulence between these two bacteria.

摘要

金黄色葡萄球菌(S. aureus)是最具临床意义的炎症诱导病原体之一,而表皮葡萄球菌(S. epidermidis)是非致病性的,在皮肤上几乎不会引起炎症。β-防御素是角蛋白细胞分泌的抗菌肽,可在受到各种微生物诱导时持续或诱导性地分泌。然而,金黄色葡萄球菌和表皮葡萄球菌在影响β-防御素产生方面的差异尚不清楚。在这项研究中,我们重点研究了金黄色葡萄球菌和表皮葡萄球菌对角蛋白细胞固有免疫反应的影响。致病性金黄色葡萄球菌主要诱导人β-防御素(hBD)1 和 hBD3,但不诱导 hBD2,而非致病性表皮葡萄球菌主要诱导人角质形成细胞产生 hBD2。从金黄色葡萄球菌上清液中制备的>10 kDa 的分子量分数诱导 hBD1 和 hBD3 的产生。另一方面,从表皮葡萄球菌上清液中制备的>100 kDa 的分子量分数诱导 hBD2 的产生。此外,表皮葡萄球菌分泌产物通过 toll 样受体(TLR)2 途径诱导 hBD2 的产生。金黄色葡萄球菌和表皮葡萄球菌的分泌产物通过不同的受体诱导 hBD 的不同亚型,这可能与这两种细菌的毒力差异有关。

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