Platelet Aggregation Induced by Strains of Various Species of Coagulase‐Negative Staphylococci

Usui, Yukio; Ohshima, Yukio; Ichiman, Yoshitoshi; Ohtomo, Toshichika; Suganuma, Masaru; Yoshida, Kenichi

doi:10.1111/j.1348-0421.1991.tb01529.x

Cited by 11 publications

(8 citation statements)

References 31 publications

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“…Enterococci-induced platelet aggregation was not inhibited by the addition of the inhibitors to arachidonate cascade. Similar results were reported in strains of CNS (41), Streptococcus sanguis (35,36), Listeria monocytogenes (9), and Aspergillus fumigatus (31). Additionally, apyrase, which hydrolyzed ADP (29), has been reported to prevent platelet aggregation induced by viridans group streptococci (35).…”

Section: Discussionsupporting

confidence: 88%

“…From the present experimental results, complement components would possibly be required in the case of enterococci, since GFP supplemented with zymosan-treated PPP lost its reactivity with these organisms remarkably. Similar results were obtained in the case of various species of CNS (41). Further, supplementation of fibrinogen, Fn, or IgG into GFP had little effect in the platelet aggregation by enterococci.…”

Section: Discussionsupporting

confidence: 83%

“…The mechanisms of platelet aggregation by these stimuli have been studied in detail (16). In contrast to these effects favorable for hemostasis, platelets also possess a pathogenic significance in disseminated intravascular coagulation (DI C) during sepsis or infective endocarditis (3,7,22,30) and observations have been made concerning the relationship between the platelet and several species of microorganisms, Staphylococcus aureus (8,18,28,40), coagulasenegative staphylococci (CNS) (41), streptococci (24,35,36,39,43), Listeria monocytogenes (9), Fusobacterium necrophorum (15), Aspergillus fumigatus (31), Candida albicans (33), Histoplasma capsulatum (10).…”

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confidence: 99%

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Platelet Aggregation by Strains of Enterococci

Usui

Ichiman

Suganuma

et al. 1991

Microbiology and Immunology

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The platelet aggregation capability of whole cells of Enterococcus faecalis, E. faecium and E. avium was tested. The optimum ratios of bacteria to platelets in E. faecali s (strain SMU-37), E. faecium (strain SMU-138) and E. avium (strain SMU-197) were 1.0, 1.2 and 2.0, respectively. During the platelet aggregation induced by the three strains of enterococci, 65-69% of total serotonin was released. The aggregation was totally inhibited by ethylenediaminetetraacetate (10 mM) and apyrase (1 mg/ml), while no effect was shown by aspirin (10 mM), indomethacin (10 mM) and quinacrine (1 mM). By pretreatment of platelet-poor plasma with heat (56 C, 30 min) or zymosan, the reactivities with platelets of each strain of species were markedly diminished. These results suggest that enterococci-induced platelet aggregation was an ion-dependent, cyclooxygenase-insensitive event, and plasma component(s) was (were) required for the reaction.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 83%

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confidence: 99%

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Platelet Aggregation by Strains of Enterococci

Usui

Ichiman

Suganuma

et al. 1991

Microbiology and Immunology

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“…The binding of Staphylococcus epidermidis was long unknown, even though it had already been shown that trypsin treatment in a culture of S. epidermidis prevented its adhesion to platelets (40), suggesting the involvement of a membrane factor. In 2009, Brennan et al showed that serine–aspartate dipeptide repeat (Sdr) G proteins expressed on the surface of S. epidermidis are necessary for the adhesion of bacteria to platelets via fibrinogen (41).…”

Section: Platelets and Bacterial Infectionsmentioning

confidence: 99%

Platelets and Infections â€“ Complex Interactions with Bacteria

et al. 2015

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Platelets can be considered sentinels of vascular system due to their high number in the circulation and to the range of functional immunoreceptors they express. Platelets express a wide range of potential bacterial receptors, including complement receptors, FcγRII, Toll-like receptors but also integrins conventionally described in the hemostatic response, such as GPIIb–IIIa or GPIb. Bacteria bind these receptors either directly, or indirectly via fibrinogen, fibronectin, the first complement C1q, the von Willebrand Factor, etc. The fate of platelet-bound bacteria is questioned. Several studies reported the ability of activated platelets to internalize bacteria such as Staphylococcus aureus or Porphyromonas gingivalis, though there is no clue on what happens thereafter. Are they sheltered from the immune system in the cytoplasm of platelets or are they lysed? Indeed, while the presence of phagolysosome has not been demonstrated in platelets, they contain antimicrobial peptides that were shown to be efficient on S. aureus. Besides, the fact that bacteria can bind to platelets via receptors involved in hemostasis suggests that they may induce aggregation; this has indeed been described for Streptococcus sanguinis, S. epidermidis, or C. pneumoniae. On the other hand, platelets are able to display an inflammatory response to an infectious triggering. We, and others, have shown that platelet release soluble immunomodulatory factors upon stimulation by bacterial components. Moreover, interactions between bacteria and platelets are not limited to only these two partners. Indeed, platelets are also essential for the formation of neutrophil extracellular traps by neutrophils, resulting in bacterial clearance by trapping bacteria and concentrating antibacterial factors but in enhancing thrombosis. In conclusion, the platelet–bacteria interplay is a complex game; its fine analysis is complicated by the fact that the inflammatory component adds to the aggregation response.

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“…The mechanism involved in S. epidermidis ‐induced platelet aggregation is unknown. It was inhibited by treatment of the bacteria with trypsin [9], suggesting that a surface protein is involved; however, the protein or proteins involved have not been identified.…”

Section: Introductionmentioning

confidence: 99%

Elucidating the role of Staphylococcus epidermidis serine–aspartate repeat protein G in platelet activation

Brennan

Loughman

Devocelle

et al. 2009

Journal of Thrombosis and Haemostasis

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Summary. Background: Staphylococcus epidermidis is a commensal of the human skin that has been implicated in infective endocarditis and infections involving implanted medical devices. S. epidermidis induces platelet aggregation by an unknown mechanism. The fibrinogen-binding protein serineaspartate repeat protein G (SdrG) is present in 67-91% of clinical strains. Objectives: To determine whether SdrG plays a role in platelet activation, and if so to investigate the role of fibrinogen in this mechanism. Methods: SdrG was expressed in a surrogate host, Lactococcus lactis, in order to investigate its role in the absence of other staphylococcal components. Platelet adhesion and platelet aggregation assays were employed. Results: L. lactis expressing SdrG stimulated platelet aggregation (lag time: 2.9 ± 0.5 min), whereas the L. lactis control did not. L. lactis SdrG-induced aggregation was inhibited by a IIb b 3 antagonists and aspirin. Aggregation was dependent on both fibrinogen and IgG, and the platelet IgG receptor FccRIIa. Preincubation of the bacteria with Bb-chain fibrinopeptide inhibited aggregation (delaying the lag time six-fold), suggesting that fibrinogen acts as a bridging molecule. Platelets adhered to L. lactis SdrG in the absence of fibrinogen. Adhesion was inhibited by a IIb b 3 antagonists, suggesting that this direct interaction involves a IIb b 3 . Investigation using purified fragments of SdrG revealed a direct interaction with the B-domains. Adhesion to the A-domain involved both a fibrinogen and an IgG bridge. Conclusion: SdrG alone is sufficient to support platelet adhesion and aggregation through both direct and indirect mechanisms.

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Platelet Aggregation Induced by Strains of Various Species of Coagulase‐Negative Staphylococci

Cited by 11 publications

References 31 publications

Platelet Aggregation by Strains of Enterococci

Platelet Aggregation by Strains of Enterococci

Platelets and Infections â€“ Complex Interactions with Bacteria

Elucidating the role of Staphylococcus epidermidis serine–aspartate repeat protein G in platelet activation

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