Statins potentiate the antibacterial effect of platelets on <i>Staphylococcus aureus</i>

Hannachi, Nadji; Fournier, Pierre‐Edouard; Martel, Hélène; Habib, Gilbert; Camoin-Jau, Laurence

doi:10.1080/09537104.2020.1792434

Cited by 9 publications

(13 citation statements)

References 26 publications

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“…The bactericidal activity observed is probably due to the action of microbicidal platelet peptides released, since the same effect is observed with the supernatant of activated platelets. We have already described this mechanism for Staphylococcus aureus [ 13 ]. These three strains of E. coli , which were sensitive to platelets, are all laboratory strains that do not express resistance mutations and are not responsible for human infectious pathologies.…”

Section: Discussionmentioning

confidence: 99%

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The Antibacterial Effect of Platelets on Escherichia coli Strains

et al. 2022

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Platelets play an important role in defense against pathogens; however, the interaction between Escherichia coli and platelets has not been well described and detailed. Our goal was to study the interaction between platelets and selected strains of E. coli in order to evaluate the antibacterial effect of platelets and to assess bacterial effects on platelet activation. Washed platelets and supernatants of pre-activated platelets were incubated with five clinical colistin-resistant and five laboratory colistin-sensitive strains of E. coli in order to study bacterial growth. Platelet activation was measured with flow cytometry by evaluating CD62P expression. To identify the difference in strain behavior toward platelets, a pangenome analysis using Roary and O-antigen serotyping was carried out. Both whole platelets and the supernatant of activated platelets inhibited growth of three laboratory colistin-sensitive strains. In contrast, platelets promoted growth of the other strains. There was a negative correlation between platelet activation and bacterial growth. The Roary results showed no logical clustering to explain the mechanism of platelet resistance. The diversity of the responses might be due to strains of different types of O-antigen. Our results show a bidirectional interaction between platelets and E. coli whose expression is dependent on the bacterial strain involved.

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Section: Discussionmentioning

confidence: 99%

“…Platelet microbicidal effects have been extensively studied for Gram-positive bacteria. It has been demonstrated that platelets decrease the growth of Staphylococcus aureus [ 13 , 14 , 15 ]. In contrast, this effect has been less studied for Gram-negative bacteria, and such data are scarce.…”

Section: Introductionmentioning

confidence: 99%

The Antibacterial Effect of Platelets on Escherichia coli Strains

et al. 2022

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“…Studies have shown that a significant number of bacterial species responsible for infections in humans can interact with platelets, causing differences in platelet activation and aggregation. It has been reported that Staphylococcus aureus and Streptococcus pyogenes rapidly attached to and aggregated on human platelets in vitro [ 2 , 3 ], whereas Escherichia coli and Enterococcus faecalis caused much slower platelet aggregation. In vitro studies have shown that some strains of bacterial species such as Fusobacterium, Listeria, Mycobacterium, Pseudomonas, Salmonella and Yersinia are able to induce platelet activation and aggregation [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

“…The mechanisms of interaction between platelets and bacteria have been widely described as in the case of Staphylococcus aureus [ 2 , 6 , 7 ]. On the other hand, they are less detailed in Gram-negative, especially E. coli .…”

Section: Introductionmentioning

confidence: 99%

Platelets and Escherichia coli: A Complex Interaction

et al. 2022

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Apart from their involvement in hemostasis, platelets have been recognized for their contribution to inflammation and defense against microbial agents. The interaction between platelets and bacteria has been well studied in the model of Staphylococcus and Streptococcus but little described in Gram-negative bacteria, especially Escherichia coli. Being involved in the hemolytic uremic syndrome as well as sepsis, it is important to study the mechanisms of interaction between platelets and E. coli. Results of the published studies are heterogeneous. It appears that some strains interact with platelets through the toll-like receptor-4 (TLR-4) and others through the Fc gamma glycoprotein. E. coli mainly uses lipopolysaccharide (LPS) to activate platelets and cause the release of antibacterial molecules, but this is not the case for all strains. In this review, we describe the different mechanisms developed in previous studies, focusing on this heterogeneity of responses that may depend on several factors; mainly, the strain studied, the structure of the LPS and the platelet form used in the studies. We can hypothesize that the structure of O-antigen and an eventual resistance to antibiotics might explain this difference.

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“…Although a great deal of research has been conducted on interactions between platelets and Gram-positive bacteria [ 5 , 6 , 7 ], which can interact with platelets indirectly via von Willebrand Factor (vWF) or directly. Staphyloccocus aureus , Streptococcus gordonii and Streptococcus sanguinis bind directly to platelets by involving proteins (SrpA, GrspB and SrpA respectively) via the platelet GPIbα [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Microscopic Description of Platelet Aggregates Induced by Escherichia coli Strains

Ezzraimi

Baudoin

Mariotti

et al. 2022

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In addition to their role in haemostasis, platelets are also involved in the inflammatory and antimicrobial process. Interactions between pathogens and platelets, mediated by receptors can lead to platelet activation, which may be responsible for a granular secretion process or even aggregation, depending on the bacterial species. Granular secretion releases peptides with bactericidal activity as well as aggregating factors. To our knowledge, these interactions have been poorly studied for Escherichia coli (E. coli). Few studies have characterised the cellular organization of platelet-E. coli aggregates. The objective of our study was to investigate the structure of platelet aggregates induced by different E. coli strains as well as the ultrastructure of platelet-E. coli mixtures using a scanning and transmission electron microscopy (SEM and TEM) approach. Our results show that the appearance of platelet aggregates is mainly dependent on the strain used. SEM images illustrate the platelet activation and aggregation and their colocalisation with bacteria. Some E. coli strains induce platelet activation and aggregation, and the bacteria are trapped in the platelet magma. However, some strains do not induce significant platelet activation and are found in close proximity to the platelets. The structure of the E. coli strains might explain the results obtained.

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Statins potentiate the antibacterial effect of platelets on Staphylococcus aureus

Cited by 9 publications

References 26 publications

The Antibacterial Effect of Platelets on Escherichia coli Strains

The Antibacterial Effect of Platelets on Escherichia coli Strains

Platelets and Escherichia coli: A Complex Interaction

Microscopic Description of Platelet Aggregates Induced by Escherichia coli Strains

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