VraSR has an important role in immune evasion of Staphylococcus aureus with low level vancomycin resistance

Gao, Cai-Hong; Dai, Yuanyuan; Chang, Wenjiao; Fang, Chao; Wang, Ziran; Ma, Xiaoling

doi:10.1016/j.micinf.2019.04.003

Cited by 14 publications

(10 citation statements)

References 33 publications

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“…It can sense cell wall damage caused by various factors and respond quickly to fix the damage, so it is considered as cell wall stimulator (Dai et al 2017). vraS/R plays an important role in low-level VAN resistance (Gao et al 2019), and some studies found that the expression of vraS/R was upregulated in the first VISA strain (named Mu50), the first hVISA strain (named Mu3) and the VISA strain (named JH9) compared to ordinary MRSA strain (Kuroda et al 2000;McAleese et al 2006). The vraS/R system involves many genes related to cell wall synthesis, including UDP-N-acetylglucosamine enolpyruvyl transferase (murZ) and monofunctional glycosyltransferase (sgtB) (Kuroda et al 2003).…”

Section: Rt-qpcr Results Of Cell-wall-related Genesmentioning

confidence: 99%

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Cell wall thickness and the molecular mechanism of heterogeneous vancomycin‐intermediateStaphylococcus aureus

Cui

Zhang

et al. 2021

Lett Appl Microbiol

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Significance and impact of the study: We isolated a heterogeneous vancomycin (VAN)-intermediate Staphylococcus aureus (hVISA) strain, and we demonstrated that the cell wall of the hVISA strain was significantly thicker than that of ordinary MRSA strains. The upregulated expression of glmS, vraR/S, sgtB, murZ and PBP4 genes related to cell wall synthesis might be the molecular mechanism underlying the cell wall thickening of the hVISA strain and might be related to its reduced sensitivity to VAN. These results could be used as a supplement to other hVISA-related studies in the world and might be beneficial to prevent and control the emergence of more hVISA.

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Section: Rt-qpcr Results Of Cell-wall-related Genesmentioning

confidence: 99%

“…vraS/R plays an important role in low‐level VAN resistance (Gao et al . 2019), and some studies found that the expression of vraS/R was upregulated in the first VISA strain (named Mu50), the first hVISA strain (named Mu3) and the VISA strain (named JH9) compared to ordinary MRSA strain (Kuroda et al . 2000; McAleese et al .…”

Section: Resultsmentioning

confidence: 99%

Cell wall thickness and the molecular mechanism of heterogeneous vancomycin‐intermediateStaphylococcus aureus

Cui

Zhang

et al. 2021

Lett Appl Microbiol

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“…The bacterial cells within the biofilm are protected against killing by antibiotics and the host immune system, leading to the increasing emergence of resistance to antimicrobial drugs and the establishment of persistent infections ( 5 ). The two-component system VraSR (vancomycin resistance-associated sensor-regulator system) positively modulates the regulation of the cell wall biosynthesis pathway in Staphylococcus aureus and plays a central role in maintaining the integrity of the cell wall peptidoglycan, antibiotic resistance against cell wall-active antibiotics, and expression of virulence factors ( 6 , 7 ). However, the mechanisms by which staphylococcal VraSR regulates biofilm formation have not been investigated in great detail.…”

Section: Introductionmentioning

confidence: 99%

“…The VraSR, as a “sentinel” system in S. aureus , is capable of rapidly sensing cell wall damage and regulating the transcription of a series of genes related to peptidoglycan synthesis ( 8 – 11 ), such as pbp2 (penicillin-binding protein), sgtB (monofunctional glycosyltransferase), and murZ (UDP- N -acetylglucosamine enolpyruvyl transferase), etc., and coordinates a response that enhances the resistance phenotype. Studies ( 12 , 13 ) have shown that the vraSR knockout mutant strain of S. aureus has decreased resistance to methicillin, vancomycin, and daptomycin cell wall antimicrobials, exhibits a thinner cell wall under a scanning electron microscope (SEM), and is more susceptible to phagocytosis by polymorphonuclear leukocytes (PMNs) ( 6 , 7 ). It is therefore possible that the inhibitor of VraSR could resensitize methicillin-resistant S. aureus (MRSA) to methicillin.…”

Section: Introductionmentioning

confidence: 99%

The Vancomycin Resistance-Associated Regulatory System VraSR Modulates Biofilm Formation of Staphylococcus epidermidis in an ica -Dependent Manner

Meng

Qian

et al. 2021

mSphere

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S. epidermidis is a leading cause of hospital-acquired catheter-related infections, and its pathogenicity depends mostly on its ability to form biofilms on implants. The biofilm formation is a complex procedure that involves multiple regulating factors. Here, we show that a vancomycin resistance-associated two-component regulatory system, VraSR, plays an important role in modulating S. epidermidis biofilm formation and tolerance to stress.

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“…TCSs typically consist of a membrane-bound sensor histidine kinase (HK) and a cytoplasmic response regulator (RR) [27,28]. TCSs have been shown to be related to bacterial resistance, bio lm synthesis and virulence [29][30][31]. For example, SaeS, an important sensor, could detect α-defendin1 (HNP-1) and response to neutrophil-derived stimuli in staphylococcus aureus [32].…”

Section: Introductionmentioning

confidence: 99%

Two-Component Signal Transduction System VraSR Contributes to Neuroinflammation in Streptococcus Suis Meningitis

Dou

Yang

et al. 2021

Preprint

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Background: Streptococcus suis (S. suis) is an important zoonotic pathogen that can cause high morbidity and mortality in both humans and swine. As the most important life-threatening infection of the central nervous system (CNS), meningitis is an important symptom of S. suis infection. The VraSR is a critical two-component signal transduction system that affects S. suis ability to resist against host innate immune system and promotes the ability of S. suis to adhere to hBMEC. Whether and how VraSR contributes to the development of S. suis meningitis are currently unknown.Methods: The in vivo colonization, in vivo BBB permeability, histopathological examination and immunohistochemistry were applied to compare and characterize the degree of destruction of brain tissue in response to wild type SC19 and mutant ΔvraSR. Western blotting and real-time PCR were combined to identify the breakdown of tight junction proteins (TJ proteins). The secretion of proinflammatory cytokines and chemokines in the serum were detected on a BD FACSVerse flow cytometer.Results: We found an important role of VraSR regulatory system in S. suis SC19-induced meningitis. A mouse infection model demonstrated that ΔvraSR had significantly attenuated inflammatory lesions in the brain tissues compared with wild-type S. suis. In vitro, we characterized that SC19 could increase the blood-brain barrier (BBB) permeability through downregulating the TJ proteins compared with mutant ΔvraSR. Moreover, we found significant generation of proinflammatory cytokines and chemokines in the serum including IL-6, TNF-α, MCP-1, and IL-12p70 compared with ΔvraSR infected mice.Conclusions: For the first time, our work investigated the VraSR regulatory system of S. suis played an important role in streptococcal meningitis and revealed VraSR to be an important contributor to the disruption of TJ proteins. Characterization of these BBB disruption will facilitate further study of meningitis mechanisms in humans, thereby offering the development of novel preventative and therapeutic strategies against infection with S. suis.

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VraSR has an important role in immune evasion of Staphylococcus aureus with low level vancomycin resistance

Cited by 14 publications

References 33 publications

Cell wall thickness and the molecular mechanism of heterogeneous vancomycin‐intermediateStaphylococcus aureus

Cell wall thickness and the molecular mechanism of heterogeneous vancomycin‐intermediateStaphylococcus aureus

The Vancomycin Resistance-Associated Regulatory System VraSR Modulates Biofilm Formation of Staphylococcus epidermidis in an ica -Dependent Manner

Two-Component Signal Transduction System VraSR Contributes to Neuroinflammation in Streptococcus Suis Meningitis

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