The Sbi Protein Contributes to Staphylococcus aureus Inflammatory Response during Systemic Infection

González, Cintia Daniela; Ledo, Camila; Giai, Constanza; Garófalo, Ailin Natalia; Gómez, M. A.

doi:10.1371/journal.pone.0131879

Cited by 21 publications

(16 citation statements)

References 43 publications

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“…Neutrophil infiltration in response to early recruited neutrophil cell death 54 is likely to be even more pronounced in infections, as many pathogens can cause necrosis of host cells 66 . Neutrophil recruitment can also be altered by pathogens that carry virulence factors that directly interfere with or promote neutrophil recruitment 67–69 . Probably one of the most important differences in infections is the presence of PAMPs (pathogen-associated molecular patterns) in addition to tissue DAMPs, creating an extra level of danger signals (reviewed in REF.…”

Section: Neutrophil Forward Migrationmentioning

confidence: 99%

Neutrophil migration in infection and wound repair: going forward in reverse

2016

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Neutrophil migration and its role during inflammation has been the focus of increased interest in the past decade. Advances in live imaging and the use of new model systems have helped to uncover the behaviour of neutrophils in injured and infected tissues. Although neutrophils were considered to be short-lived effector cells that undergo apoptosis in damaged tissues, recent evidence suggests that neutrophil behaviour is more complex and, in some settings, neutrophils might leave sites of tissue injury and migrate back into the vasculature. The role of reverse migration and its contribution to resolution of inflammation remains unclear. Here, we discuss the different cues within tissues that mediate neutrophil forward and reverse migration in response to injury or infection, and the implications of these mechanisms to human disease.

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Section: Neutrophil Forward Migrationmentioning

confidence: 99%

Neutrophil migration in infection and wound repair: going forward in reverse

2016

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“…Proteins identified exclusively on the surface of virulent strain CH21 include immunoglobulin-binding protein (Sbi) and N-acetylmuramoyl-L-alanine amidase (Y2979; BJL64_14035). Sbi and staphylococcal protein A (SpA) are IgG binders with a demonstrated role in staphylococcal virulence (Gonzalez et al, 2015 ). While SpA binds Fcγ of IgGs, Sbi has two Ig-binding domains and two domains that bind to complement component C3 (Zhao et al, 2016 ).…”

Section: Resultsmentioning

confidence: 99%

Joint Genomic and Proteomic Analysis Identifies Meta-Trait Characteristics of Virulent and Non-virulent Staphylococcus aureus Strains

Bonar

Bukowski

Hydzik

et al. 2018

Front. Cell. Infect. Microbiol.

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Staphylococcus aureus is an opportunistic pathogen of humans and warm-blooded animals and presents a growing threat in terms of multi-drug resistance. Despite numerous studies, the basis of staphylococcal virulence and switching between commensal and pathogenic phenotypes is not fully understood. Using genomics, we show here that S. aureus strains exhibiting virulent (VIR) and non-virulent (NVIR) phenotypes in a chicken embryo infection model genetically fall into two separate groups, with the VIR group being much more cohesive than the NVIR group. Significantly, the genes encoding known staphylococcal virulence factors, such as clumping factors, are either found in different allelic variants in the genomes of NVIR strains (compared to VIR strains) or are inactive pseudogenes. Moreover, the pyruvate carboxylase and gamma-aminobutyrate permease genes, which were previously linked with virulence, are pseudogenized in NVIR strain ch22. Further, we use comprehensive proteomics tools to characterize strains that show opposing phenotypes in a chicken embryo virulence model. VIR strain CH21 had an elevated level of diapolycopene oxygenase involved in staphyloxanthin production (protection against free radicals) and expressed a higher level of immunoglobulin-binding protein Sbi on its surface compared to NVIR strain ch22. Furthermore, joint genomic and proteomic approaches linked the elevated production of superoxide dismutase and DNA-binding protein by NVIR strain ch22 with gene duplications.

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“…The second immunoglobulin-binding protein (Sbi), is found anchored in the membrane and extracellularly (93). Sbi is a pro-inflammatory staphylococcal antigen (94) and both forms contribute to S. aureus immune evasion (phagocytosis and Neutrophil killing) (93). In addition to the increased protease and hemolysins production observed, decreased production of Sbi in JE2 Δ rpiRc would suggest increased virulence for this mutant in vivo as previously observed in two in vivo mouse models of abscess and pneumonia using planktonic bacteria (75, 76).…”

Section: Discussionmentioning

confidence: 99%

RpiRc regulates RsbU to modulate eDNA-dependent biofilm formation andin vivovirulence ofStaphylococcus aureusin a mouse model of catheter infection

Fischer

Girard

Laumay

et al. 2019

Preprint

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15Staphylococcus aureus is a major human pathogen. Despite high incidence and morbidity, molecular 16 mechanisms occurring during infection remain largely unknown. Under defined conditions, biofilm 17 formation contributes to the severity of S. aureus related infections. Extracellular DNA (eDNA), a 18 component of biofilm matrix released from apoptotic bacteria, is involved in biofilm structure and 19 stability. In many bacterial biofilms, eDNA originates from cell lysis although eDNA can also be 20 actively secreted or exported by bacterial membrane vesicles. By screening the Nebraska transposon 21 library, we identified rpiRc as a biofilm regulator involved in eDNA regulation. RpiRc is a transcription 22 factor from the pentose phosphate pathway (PPP) whose product is a polysaccharide intercellular 23 adhesin (PIA) precursor. However, rpiRc mutant strain showed neither susceptibility to DispersinB® (a 24 commercially available enzyme disrupting PIA biofilms) nor alteration of ica transcription (the operon 25 regulating PIA production). Decreased biofilm formation was linked to Sln, an extracellular compound 26 degrading eDNA in an autolysis independent pathway. Biofilm susceptibility to antibiotics in wt and 27 mutant strains was tested using a similar protocol as the Calgary biofilm device. Involvement of RpiRc 28 in S. aureus virulence was assessed ex vivo by internalization experiments into HEK293 cells and in 29 vivo in a mouse model of subcutaneous catheter infection. While minimum inhibitory concentrations 30 (MICs) of planktonic cells were not affected in the mutant strain, we observed increased biofilm 31 susceptibility to almost all tested antibiotics, regardless of their mode of action. More importantly, 32 the rpiRc mutant showed reduced virulence in both ex vivo and in vivo experiments related to 33 decreased fnbpA-B transcription and eDNA production. RpiRc is an important regulator involved in 34 eDNA degradation inside the matrix of mature PIA independent biofilms. These results illustrate that 35 RpiRc contributes to increased antibiotic tolerance in mature bacterial biofilm and also to S. aureus 36 cell adhesion and virulence during subcutaneous infection. 37 38 3 39 Author summary 40 Biofilm formation contributes to the severity of Staphylococcus aureus related infections. Biofilm 41 matrix is mainly composed by polysaccharide intercellular adhesion (PIA), proteins and extracellular 42 DNA (eDNA). By screening a mutant library of S. aureus, RpiRc was identified as a new regulator of 43 eDNA dependent biofilm formation. How RpiRc regulates biofilm and its role in S. aureus virulence 44 was studied in four different S. aureus strains. Deletion of RpiRc resulted in a pronounced decreased 45 eDNA dependent biofilm formation, but not PIA dependent biofilm formation. Decreased biofilm 46 formation was not related to increased autolysis, but was linked to extracellular compounds found in 47 the supernatant of mutant biofilms. Sln was identified as one of this compound. RpiRc deletion also 48 decreased...

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The Sbi Protein Contributes to Staphylococcus aureus Inflammatory Response during Systemic Infection

Cited by 21 publications

References 43 publications

Neutrophil migration in infection and wound repair: going forward in reverse

Neutrophil migration in infection and wound repair: going forward in reverse

Joint Genomic and Proteomic Analysis Identifies Meta-Trait Characteristics of Virulent and Non-virulent Staphylococcus aureus Strains

RpiRc regulates RsbU to modulate eDNA-dependent biofilm formation andin vivovirulence ofStaphylococcus aureusin a mouse model of catheter infection

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