Pathogen activators of plasminogen

Verhamme, Ingrid M.; Panizzi, Peter; Bock, Paul E.

doi:10.1111/jth.12939

Cited by 22 publications

(11 citation statements)

References 62 publications

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“…This work established that S. aureus exploits the host factors prothrombin and fibrinogen to induce the formation of fibrin agglutinates and shield bacteria from phagocytes [16]. Enumeration of S. aureus in blood requires release of bacteria from fibrin cables, which is achieved by treating samples with streptokinase, an activator of plasminogen [30]. When incubated in fresh human blood, approximately 99% of the inoculum of S. simulans carrying vector alone (1.25×10 7 CFU) was killed within 60 min (Fig.…”

Section: Resultsmentioning

confidence: 99%

Pathogenic conversion of coagulase-negative staphylococci

Kim

Rauch

et al. 2017

Microbes and Infection

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Humans and animals are colonized by members of the genus Staphylococcus, however only some of these species evolved to cause invasive disease. The genetic basis for conversion of commensal staphylococci into pathogens is not known. We hypothesized that Staphylococcus aureus genes for coagulation and agglutination in vertebrate blood (coa, vwb and clfA) may support pathogenic conversion. Expression of coa and vwb in Staphylococcus epidermidis or Staphylococcus simulans supported a coagulase-positive phenotype but not the ability to cause disease in a mouse model of bloodstream infection. However, the simultaneous expression of coa, vwb and clfA in coagulase-negative staphylococci enabled bacterial agglutination in plasma and enhanced survival of S. simulans in human whole blood. Agglutination of S. simulans in the bloodstream of infected mice upon expression of coa, vwb and clfA provided also a mean for dissemination and replication in distal organs. Thus, the acquisition of genes for bacterial agglutination with fibrin appear sufficient for the conversion of commensal staphylococci into invasive pathogens.

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Section: Resultsmentioning

confidence: 99%

Pathogenic conversion of coagulase-negative staphylococci

Kim

Rauch

et al. 2017

Microbes and Infection

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“…Invasion by S. eriocheiris was decreased after competitive inhibition by SeEnolase. Enolase has been reported to play a role as plasminogen receptor on the surface of several pathogenic bacteria (38, 39), fungi (40), and protozoa (41–43). For example, in Vibrio parahaemolyticus , the glycolytic enzyme enolase, a membrane associated protein located on the cell surface was found to bind plasminogen (28).…”

Section: Discussionmentioning

confidence: 99%

Spiroplasma eriocheiris Invasion Into Macrobrachium rosenbergii Hemocytes Is Mediated by Pathogen Enolase and Host Lipopolysaccharide and β-1, 3-Glucan Binding Protein

et al. 2019

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Spiroplasma eriocheiris is a crustacean pathogen, without a cell wall, that causes enormous economic loss. Macrobrachium rosenbergii hemocytes are the major targets during S. eriocheiris infection. As wall-less bacteria, S. eriocheiris , its membrane protein should interact with host membrane protein directly and firstly when invaded in host cell. In this investigation, six potential hemocyte receptor proteins were identified firstly that mediate interaction between S. eriocheiris and M. rosenbergii . Among these proteins, lipopolysaccharide and β-1, 3-glucan binding protein (MrLGBP) demonstrated to bind to S. eriocheiris using bacterial binding assays and confocal microscopy. Four spiroplasma ligand proteins for MrLGBP were isolated and identified. But, competitive assessment demonstrated that only enolase of S. eriocheiris (SeEnolase) could be a candidate ligand for MrLGBP. Subsequently, the interaction between MrLGBP and SeEnolase was confirmed by co-immunoprecipitation and co-localization in vitro . After the interaction between MrLGBP and SeEnolase was inhibited by antibody neutralization test, the virulence ability of S. eriocheiris was effectively reduced. The quantity of S. eriocheiris decreased in Drosophila S2 cells after overexpression of MrLGBP , compared with the controls. In addition, RNA interference (RNAi) knockdown of MrLGBP made M. rosenbergii more sensitive to S. eriocheiris infection. Further studies found that the immune genes, including MrLGBP and prophenoloxidase ( MrproPO ), MrRab7A , and Mrintegrin α 1 were significantly up-regulated by SeEnolase stimulation. After SeEnolase pre-stimulation, the ability of M. rosenbergii resistance to S. eriocheiris was significantly improved. Collectively, this investigation demonstrated that MrLGBP and pathogen SeEnolase involved in mediating S. eriocheiris invasion into M. rosenbergii hemocytes.

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“…S. agalactiae pathogenesis likely includes SkzL to enhance bacterial spreading through fibrinolytic enhancement. These are prime examples of pathogens exerting virulence by hijacking the host coagulation and fibrinolytic systems [188]. …”

Section: Proteases and Diseasementioning

confidence: 99%

Proteases: Pivot Points in Functional Proteomics

Verhamme

Leonard

Perkins

2018

Functional Proteomics

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Proteases drive the life cycle of all proteins, ensuring the transportation and activation of newly minted, would-be proteins into their functional form while recycling spent or unneeded proteins. Far from their image as engines of protein digestion, proteases play fundamental roles in basic physiology and regulation at multiple levels of systems biology. Proteases are intimately associated with disease and modulation of proteolytic activity is the presumed target for successful therapeutics. “Proteases: Pivot Points in Functional Proteomics” examines the crucial roles of proteolysis across a wide range of physiological processes and diseases. The existing and potential impacts of proteolysis-related activity on drug and biomarker development are presented in detail. All told the decisive roles of proteases in four major categories comprising 23 separate sub-categories are addressed. Within this construct, 15 sets of subject-specific, tabulated data are presented that include identification of proteases, protease inhibitors, substrates and their actions. Said data are derived from and confirmed by over 300 references. Cross comparison of datasets indicates that proteases, their inhibitors/promoters and substrates intersect over a range of physiological processes and diseases, both chronic and pathogenic. Indeed, “Proteases: Pivot Points …” closes by dramatizing this very point through association of (pro)Thrombin and Fibrin(ogen) with: hemostasis, innate immunity, cardiovascular and metabolic disease, cancer, neurodegeneration and bacterial self-defense.

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Pathogen activators of plasminogen

Cited by 22 publications

References 62 publications

Pathogenic conversion of coagulase-negative staphylococci

Pathogenic conversion of coagulase-negative staphylococci

Spiroplasma eriocheiris Invasion Into Macrobrachium rosenbergii Hemocytes Is Mediated by Pathogen Enolase and Host Lipopolysaccharide and β-1, 3-Glucan Binding Protein

Proteases: Pivot Points in Functional Proteomics

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