Platelets and Escherichia coli: A Complex Interaction

Abstract

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.

Platelet P2Y12 signalling pathway in the dysregulated immune response during sepsis

“…On the contrary, bacteria that enter the bloodstream, such as S. epidermidis and Streptococcus pneumoniae , do not induce permanent platelet aggregation (Yeaman, 2010). These data indicate that pathogen‐induced platelet activation and aggregation rely on the strain of bacteria, platelet‐to‐bacteria ratio and platelet variability between individuals and these factors influence the host's ability to fight off pathogens (Ezzeroug Ezzraimi et al, 2022). Consequently, antiplatelet therapy targeting receptor P2Y 12 can contribute to regulating platelet–pathogen interaction in sepsis.…”

Prevalence of Extended-Spectrum B-Lactamase (ESBL) and Quinolone Resistance (qnr) Genes among Cytotoxic Necrotizing Factor-1-Producing Uropathogenic Escherichia coli in Babylon, Iraq

“…A considerable range of nosocomial infections is caused by Escherichia coli (E. coli) [1] . In spite of being as a member of the normal flora of humans and wildlife, [2] E. coli isolates cause urinary and gastrointestinal tract infections (UTI and GIT, respectively), skin and respiratory infections, sepsis, and neonatal meningitis [3][4][5] . Infections could range from severe or lethal to insignificant depending on the level of antibiotic resistance and encoding of bacterial virulence factors.…”

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Microscopic Description of Platelet Aggregates Induced by Escherichia coli Strains

“…The data on Gram-negative bacteria, in particular Escherichia coli , remain insufficient to understand the molecular mechanism of these interactions and to understand the factor of variability of the results. This interaction has been shown to be primarily dependent on TLR4 binding with LPS or by FcγRII recruitment [ 8 ].…”

“…We also observed a correlation between this bactericidal effect and the capacity of strains to induce platelet activation [ 9 ]. Indeed, some E. coli strains induced platelet activation, a result that brought into question the platelet aggregation capability of these strains [ 8 , 9 ].…”