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脂蛋白成熟在2型血清型所致感染发病机制中的作用。

Role of Maturation of Lipoproteins in the Pathogenesis of the Infection Caused by Serotype 2.

作者信息

Payen Servane, Roy David, Boa Anaïs, Okura Masatoshi, Auger Jean-Philippe, Segura Mariela, Gottschalk Marcelo

机构信息

Swine and Poultry Infectious Diseases Research Center (CRIPA) and Research Group on Infectious Diseases in Production Animals (GREMIP), Faculty of Veterinary Medicine, University of Montreal, Saint-Hyacinthe, QC J2S 2M2, Canada.

Division of Bacterial and Parasitic Disease, National Institute of Animal Health, National Agriculture and Food Research Organization, Tsukuba 305-0856, Japan.

出版信息

Microorganisms. 2021 Nov 19;9(11):2386. doi: 10.3390/microorganisms9112386.

DOI:10.3390/microorganisms9112386
PMID:34835511
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8621357/
Abstract

serotype 2 is an important porcine bacterial pathogen associated with multiple pathologies in piglets. Bacterial lipoproteins (LPPs) have been described as playing important roles in the pathogenesis of the infection of other Gram-positive bacteria as adhesins, pro-inflammatory cell activators and/or virulence factors. In the current study, we aimed to evaluate the role of the prolipoprotein diacylglyceryl transferase (Lgt) and lipoprotein signal peptidase (Lsp) enzymes, which are responsible for LPP maturation, on the pathogenesis of the infection caused by two different sequence types (STs) of serotype 2 strains (virulent ST1 and highly virulent ST7). Through the use of isogenic Δ, Δ and double Δ/Δ mutants, it was shown that lack of these enzymes did not influence adhesion/invasion to porcine respiratory epithelial cells. However, in the absence of the Lsp and/or Lgt, a significant reduction in the capacity of to activate phagocytic cells and induce pro-inflammatory mediators (in vitro and in vivo) was observed. In general, results obtained with the double mutant did not differ in comparison to single mutants, indicating lack of an additive effect. Finally, our data suggest that these enzymes play a differential role in virulence, depending on the genetic background of the strain and being more important for the highly virulent ST7 strain.

摘要

血清型2是一种重要的猪源细菌病原体,与仔猪的多种病理状况相关。细菌脂蛋白(LPPs)已被描述为在其他革兰氏阳性菌感染的发病机制中发挥重要作用,如作为黏附素、促炎细胞激活剂和/或毒力因子。在本研究中,我们旨在评估负责LPP成熟的前脂蛋白二酰甘油转移酶(Lgt)和脂蛋白信号肽酶(Lsp)在血清型2菌株的两种不同序列类型(STs)(强毒株ST1和高毒力株ST7)引起的感染发病机制中的作用。通过使用同基因的Δlgt、Δlsp和双Δlgt/Δlsp突变体,结果表明缺乏这些酶并不影响对猪呼吸道上皮细胞的黏附/侵袭。然而,在缺乏Lsp和/或Lgt的情况下,观察到激活吞噬细胞和诱导促炎介质的能力(体外和体内)显著降低。总体而言,双突变体获得的结果与单突变体相比没有差异,表明不存在累加效应。最后,我们的数据表明,这些酶在毒力方面发挥不同作用,这取决于菌株的遗传背景,并且对高毒力的ST7菌株更为重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/c543880d2114/microorganisms-09-02386-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/f04c74223ce3/microorganisms-09-02386-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/0310402398ee/microorganisms-09-02386-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/00ed1bbd8332/microorganisms-09-02386-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/4999327a0f49/microorganisms-09-02386-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/b6376fecaea5/microorganisms-09-02386-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/b9a92cbf4973/microorganisms-09-02386-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/38155834506c/microorganisms-09-02386-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/a42adad092c5/microorganisms-09-02386-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/c543880d2114/microorganisms-09-02386-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/f04c74223ce3/microorganisms-09-02386-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/0310402398ee/microorganisms-09-02386-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/00ed1bbd8332/microorganisms-09-02386-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/4999327a0f49/microorganisms-09-02386-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/b6376fecaea5/microorganisms-09-02386-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/b9a92cbf4973/microorganisms-09-02386-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/38155834506c/microorganisms-09-02386-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/a42adad092c5/microorganisms-09-02386-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28a5/8621357/c543880d2114/microorganisms-09-02386-g009.jpg

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