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Open AccessArticle

Streptococcus suis Uptakes Carbohydrate Source from Host Glycoproteins by N-glycans Degradation System for Optimal Survival and Full Virulence during Infection

by Jiale Ma 1,2,3,†, Ze Zhang 1,2,3,†, Zihao Pan 1,2,3, Qiankun Bai 1,2,3, Xiaojun Zhong 1,2,3, Yinchu Zhu 1,2,3, Yue Zhang 1,2,3, Zongfu Wu 1,2,3, Guangjin Liu 1,2,3 and Huochun Yao 1,2,3,*
1
MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China
2
Key Lab of Animal Bacteriology, Ministry of Agriculture, Nanjing 210095, China
3
OIE Reference Lab for Swine Streptococcosis, Nanjing 210095, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Pathogens 2020, 9(5), 387; https://doi.org/10.3390/pathogens9050387
Received: 24 March 2020 / Revised: 12 May 2020 / Accepted: 14 May 2020 / Published: 18 May 2020
Infection with the epidemic virulent strain of Streptococcus suis serotype 2 (SS2) can cause septicemia in swine and humans, leading to pneumonia, meningitis and even cytokine storm of Streptococcal toxic shock-like syndrome. Despite some progress concerning the contribution of bacterial adhesion, biofilm, toxicity and stress response to the SS2 systemic infection, the precise mechanism underlying bacterial survival and growth within the host bloodstream remains elusive. Here, we reported the SS2 virulent strains with a more than 20 kb endoSS-related insertion region that showed significantly higher proliferative ability in swine serum than low-virulent strains. Further study identified a complete N-glycans degradation system encoded within this insertion region, and found that both GH92 and EndoSS contribute to bacterial virulence, but that only DndoSS was required for optimal growth of SS2 in host serum. The supplement of hydrolyzed high-mannose-containing glycoprotein by GH92 and EndoSS could completely restore the growth deficiency of endoSS deletion mutant in swine serum. EndoSS only hydrolyzed a part of the model glycoprotein RNase B with high-mannose N-linked glycoforms into a low molecular weight form, and the solo activity of GH92 could not show any changes comparing with the blank control in SDS-PAGE gel. However, complete hydrolyzation was observed under the co-incubation of EndoSS and GH92, suggesting GH92 may degrade the high-mannose arms of N-glycans to generate a substrate for EndoSS. In summary, these findings provide compelling evidences that EndoSS-related N-glycans degradation system may enable SS2 to adapt to host serum-specific availability of carbon sources from glycoforms, and be required for optimal colonization and full virulence during systemic infection. View Full-Text
Keywords: Streptococcus suis; N-glycans degradation system; EndoSS; GH92; serum growth; virulence Streptococcus suis; N-glycans degradation system; EndoSS; GH92; serum growth; virulence
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Ma, J.; Zhang, Z.; Pan, Z.; Bai, Q.; Zhong, X.; Zhu, Y.; Zhang, Y.; Wu, Z.; Liu, G.; Yao, H. Streptococcus suis Uptakes Carbohydrate Source from Host Glycoproteins by N-glycans Degradation System for Optimal Survival and Full Virulence during Infection. Pathogens 2020, 9, 387.

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