Inactivation of Dipeptidyl Peptidase IV Attenuates the Virulence of Streptococcus suis Serotype 2 that Causes Streptococcal Toxic Shock Syndrome
Inactivation of Dipeptidyl Peptidase IV Attenuates the Virulence of Streptococcus suis Serotype 2 that Causes Streptococcal Toxic Shock Syndrome
复制标题
二肽基肽酶 IV 失活可减弱引起链球菌中毒性休克综合征的猪链球菌血清型 2 的毒力
DOI：
10.1007/s00284-009-9425-8
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发表时间：
2009-09-01
影响因子：
2.6
通讯作者：
Tang, Jiaqi
中科院分区：
文献类型：
--
作者：
Ge, Junchao;Feng, Youjun;Tang, Jiaqi
二肽基肽酶IV（Dipeptidyl peptidase IV，DPP IV）是一种在真核细胞中被识别为CD26的酶，广泛存在于猪链球菌（Streptococcus suis，S. suis），一种新兴的人畜共患病原体。然而，DPP IV在S.猪的毒力仍不清楚。在这里，我们从高度侵袭性的S.猪链球菌2型（SS2）引起链球菌中毒性休克综合征（STSS）。酶促分析再现了dpp IV蛋白产物作为功能性DPP IV的酶促活性，并且ELISA分析证明SS2 DPP IV可以与人纤连蛋白相互作用。通过同源重组获得了dpp IV的SS2等基因突变体Delta dpp IV。实验动物感染表明，dpp IV的灭活大大减弱了SS2中国强毒株的高毒力。功能互补可以恢复SS2致病性的这一缺陷。据我们所知，这可能首次证实DPP IV有助于SS2毒力。
Di-peptidyl peptidase IV (DPP IV), originally recognized as CD26 in eukaryotic cells, is distributed widely in microbial pathogens, including Streptococcus suis (S. suis), an emerging zoonotic agent. However, the role of DPP IV in S. suis virulence remains unclear. Here, we identified a dpp IV homologue from highly invasive isolate of S. suis 2 (SS2) causing streptococcal toxic shock syndrome (STSS). Enzymatic assays reproduced its enzymatic activity of dpp IV protein product as a functional DPP IV, and ELISA analysis demonstrated that SS2 DPP IV can interact with human fibronectin. An isogenic SS2 mutant of dpp IV, Delta dpp IV, was obtained by homologous recombination. Experimental animal infection suggested that an inactivation of dpp IV attenuates greatly its high virulence of Chinese virulent strains of SS2. Functional complementation can restore this defect in SS2 pathogenicity. To our knowledge, it may confirm, for the first time, that DPP IV contributes to SS2 virulence.