↓ Skip to main content

Roles of the Putative Type IV-like Secretion System Key Component VirD4 and PrsA in Pathogenesis of Streptococcus suis Type 2

Overview of attention for article published in Frontiers in Cellular and Infection Microbiology, December 2016
Altmetric Badge

About this Attention Score

  • Average Attention Score compared to outputs of the same age and source

Mentioned by

twitter
2 X users

Citations

dimensions_citation
34 Dimensions

Readers on

mendeley
21 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
Roles of the Putative Type IV-like Secretion System Key Component VirD4 and PrsA in Pathogenesis of Streptococcus suis Type 2
Published in
Frontiers in Cellular and Infection Microbiology, December 2016
DOI 10.3389/fcimb.2016.00172
Pubmed ID
Authors

Xiaowu Jiang, Yunkai Yang, Jingjing Zhou, Lexin Zhu, Yuanxing Gu, Xiaoyan Zhang, Xiaoliang Li, Weihuan Fang

Abstract

Streptococcus suis type 2 (SS2) is a zoonotic pathogen causing septic infection, meningitis and pneumonia in pigs and humans. SS2 may cause streptococcal toxic shock syndrome (STSS) probably due to excessive release of inflammatory cytokines. A previous study indicated that the virD4 gene in the putative type IV-like secretion system (T4SS) within the 89K pathogenicity island specific for recent epidemic strains contributed to the development of STSS. However, the functional basis of VirD4 in STSS remains unclear. Here we show that deletion of virD4 led to reduced virulence as shown by about 65% higher LD50, lower bacterial load in liver and brain, and lower level of expression of inflammatory cytokines in mice and cell lines than its parent strain. The ΔVirD4 mutant was more easily phagocytosed, suggesting its role as an anti-phagocytic factor. Oxidative stress that mimic bacterial exposure to respiratory burst of phagocytes upregulated expression of virD4. Proteomic analysis identified 10 secreted proteins of significant differences between the parent and mutant strains under oxidative stress, including PrsA, a peptidyl-prolyl isomerase. The SS2 PrsA expressed in E. coli caused a dose-dependent cell death and increased expression of proinflammatory IL-1β, IL-6 and TNF-α in murine macrophage cells. Our data provide novel insights into the contribution of the VirD4 factor to STSS pathogenesis, possibly via its anti-phagocytic activity, upregulation of its expression upon oxidative stress and its involvement in increased secretion of PrsA as a cell death inducer and proinflammatory effector.

Timeline

Login to access the full chart related to this output.

If you don’t have an account, click here to discover Explorer

X Demographics

X Demographics

The data shown below were collected from the profiles of 2 X users who shared this research output. Click here to find out more about how the information was compiled.
As of 1 July 2024, you may notice a temporary increase in the numbers of X profiles with Unknown location. Click here to learn more.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 21 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 21 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 24%
Student > Master 5 24%
Student > Bachelor 2 10%
Student > Doctoral Student 1 5%
Professor 1 5%
Other 4 19%
Unknown 3 14%
Readers by discipline Count As %
Medicine and Dentistry 4 19%
Biochemistry, Genetics and Molecular Biology 4 19%
Veterinary Science and Veterinary Medicine 3 14%
Immunology and Microbiology 3 14%
Agricultural and Biological Sciences 2 10%
Other 0 0%
Unknown 5 24%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 02 December 2016.
All research outputs
#19,944,994
of 25,374,647 outputs
Outputs from Frontiers in Cellular and Infection Microbiology
#5,133
of 8,068 outputs
Outputs of similar age
#297,557
of 416,039 outputs
Outputs of similar age from Frontiers in Cellular and Infection Microbiology
#34
of 75 outputs
Altmetric has tracked 25,374,647 research outputs across all sources so far. This one is in the 18th percentile – i.e., 18% of other outputs scored the same or lower than it.
So far Altmetric has tracked 8,068 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.8. This one is in the 25th percentile – i.e., 25% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 416,039 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 24th percentile – i.e., 24% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 75 others from the same source and published within six weeks on either side of this one. This one is in the 42nd percentile – i.e., 42% of its contemporaries scored the same or lower than it.