Hyaluronate lyase activity of Streptococcus suis serotype 2 and modulatory effects of hyaluronic acid on the bacterium's virulence properties.

Hyaluronate lyase activity of Streptococcus suis serotype 2 and modulatory effects of hyaluronic acid on the bacterium's virulence properties.
复制标题

DOI:
10.1186/s13104-015-1692-9
复制
发表时间:
2015-11-26
期刊:
影响因子:
1.8
通讯作者:
Grenier D
Grenier D
中科院分区:
其他
文献类型:
--
作者:
Haas B;Vaillancourt K;Bonifait L;Gottschalk M;Grenier D

文献摘要

被引文献

相似文献

猪链球菌血清2型是世界范围内主要的猪病原体和人畜共患病原体,主要引起脑膜炎和败血症。透明质酸分解酶是一种降解透明质酸的酶,透明质酸是动物组织的主要成分,据报道,它是多种细菌的毒力因子。由于猪链球菌的透明质酸裂解酶一直被模糊地认为是一种毒力因子,我们从北美发现的三种主要克隆复合体(序列型[ST] 1、ST25和ST28)中筛选出50株已知毒力程度不同的分离株,以便将这种活性的存在或不存在与毒力程度联系起来。此外,我们还研究了外源性透明质酸对猪链球菌毒力因子基因表达和脑大血管内皮细胞(BMEC)促炎反应的影响。我们发现除了一个ST1分离株(高毒力)外,所有的ST25(中毒力)和ST28(低毒力)分离株都具有透明质酸裂解酶活性。一个2bp的插入是ST1菌株缺乏活性的原因。由于最毒的分离株不降解透明质酸,这种组织成分可能在感染过程中被发现。因此,我们研究了其对猪链球菌和宿主细胞的影响。透明质酸可调节猪链球菌对BMEC的粘附,增加猪链球菌毒力因子的表达,并促进BMEC分泌促炎细胞因子。这些发现表明猪链球菌透明质酸裂解酶在其活性形式下并不代表一个关键的毒力因子。然而,在感染过程中,外源性透明质酸可能与猪链球菌和宿主细胞相互作用,除了促进炎症外,似乎还可以调节细菌的几个毒力决定因素。本文的在线版本(doi:10.1186/s13104-015-1692-9)包含补充材料,可供授权用户使用。
Streptococcus suis serotype 2 is a major swine pathogen and zoonotic agent worldwide causing mainly meningitis and septicemia. Hyaluronate lyases are enzymes that degrade hyaluronic acid, a major constituent of animal tissues, and have been reported as virulence factors in various bacterial species. Since the hyaluronate lyase of S. suis has been considered ambiguously as a virulence factor, we screened 50 isolates from the three major clonal complexes found in North America (sequence type [ST] 1, ST25, and ST28) known to differ in their degree of virulence in order to link the presence or absence of this activity with the degree of virulence. Moreover, the effect of exogenous hyaluronic acid on S. suis virulence factor gene expression and the pro-inflammatory response of brain macrovascular endothelial cells (BMEC) was also investigated. We found that all but one ST1 isolates (high virulence) were devoid of hyaluronate lyase activity whereas all ST25 (intermediate virulence) and ST28 (low virulence) isolates possessed the activity. A 2 bp insertion was responsible for the lack of activity in ST1 strains. Since the most virulent isolates did not degrade hyaluronic acid, this tissue component may be found during the infectious process. Therefore, we investigated its effect on S. suis and host cells. Hyaluronic acid was found to modulate S. suis adhesion to BMEC, to increase S. suis virulence factor expression, and to enhance pro-inflammatory cytokine secretion by BMEC. These findings suggest that S. suis hyaluronate lyase does not represent a critical virulence factor in its active form. However, exogenous hyaluronic acid that is likely to interact with S. suis and host cells during the course of infection appears to modulate several virulence determinants of the bacterium, in addition to promote inflammation. The online version of this article (doi:10.1186/s13104-015-1692-9) contains supplementary material, which is available to authorized users.