[The role of blood platelets in infections].

Platelets are primarily associated with their main function, hemostasis, although it is known that these cells also exhibit biological activity in cancer progression, inflammation and infectious processes. During infection platelets, due to the expression of specific receptors - Toll-like receptors (TLRs) - which recognize molecular patterns associated with pathogens - pathogen-associated molecular patterns (PAMPs) - are activated by the presence of microorganism components and/or substances released from damaged cells/tissue. Further antimicrobial activity of platelets is based on their capacity for phagocytosis, generation of reactive oxygen species (ROS), and the synthesis, storage and release of proteins/peptides with antimicrobial activity. Another mechanism of platelet action is their immunomodulatory activity. It is based mainly on the ability to secrete chemotactic factors allowing the accumulation of professional immunocompetent cells at the site of infection, thus enhancing the effective eradication of an infectious agent. In chronic infections, platelets, due to release of numerous growth factors and various cytokines, support mechanisms of acquired immunity. They accelerate the maturation of dendritic cells, stimulate B cells to be immunoglobulin-producing plasma cells and potentiate the activity of T cells. Unfortunately, in certain situations (the existence of specific risk factors) the interaction of microorganisms with activated platelets may also be the cause of pathology within the cardiovascular system.

[1]  B. Sadowska,et al.  Antimicrobial/anti-biofilm activity of expired blood platelets and their released products. , 2013, Postepy higieny i medycyny doswiadczalnej.

[2]  D. Missiakas,et al.  Recurrent infections and immune evasion strategies of Staphylococcus aureus. , 2012, Current opinion in microbiology.

[3]  P. Kubes,et al.  Innate immunity in the vasculature: interactions with pathogenic bacteria. , 2012, Current opinion in microbiology.

[4]  M. Rasmussen,et al.  Platelet and Neutrophil Responses to Gram Positive Pathogens in Patients with Bacteremic Infection , 2011, PloS one.

[5]  D. Missiakas,et al.  Preventing Staphylococcus aureus Sepsis through the Inhibition of Its Agglutination in Blood , 2011, PLoS pathogens.

[6]  S. Watson,et al.  Platelets and the innate immune system: mechanisms of bacterial‐induced platelet activation , 2011, Journal of thrombosis and haemostasis : JTH.

[7]  Benquan Wu,et al.  Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation , 2011, Inflammation Research.

[8]  O. Garraud,et al.  Pathogen sensing, subsequent signalling, and signalosome in human platelets. , 2011, Thrombosis research.

[9]  D. Newby,et al.  Platelet receptor polymorphisms do not influence Staphylococcus aureus–platelet interactions or infective endocarditis , 2011, Microbes and infection.

[10]  K. Werdan,et al.  Staphylococcus aureus α-Toxin Triggers the Synthesis of B-Cell Lymphoma 3 by Human Platelets , 2011, Toxins.

[11]  A. Antczak,et al.  Internalization of IgG-Coated Targets Results in Activation and Secretion of Soluble CD40 Ligand and RANTES by Human Platelets , 2010, Clinical and Vaccine Immunology.

[12]  M. Mörgelin,et al.  Clinical isolates of Enterococcus faecalis aggregate human platelets. , 2010, Microbes and infection.

[13]  A. Dardik,et al.  Platelet-Rich Plasma: Support for Its Use in Wound Healing , 2010, The Yale journal of biology and medicine.

[14]  D. Cox,et al.  Platelet–bacterial interactions , 2010, Cellular and Molecular Life Sciences.

[15]  A. Bayer,et al.  Factors influencing time to vancomycin-induced clearance of nonendocarditis methicillin-resistant Staphylococcus aureus bacteremia: role of platelet microbicidal protein killing and agr genotypes. , 2010, The Journal of infectious diseases.

[16]  M. Yeaman Platelets in defense against bacterial pathogens , 2009, Cellular and Molecular Life Sciences.

[17]  T. Shaw,et al.  Wound repair at a glance , 2009, Journal of Cell Science.

[18]  M. Klinger,et al.  The blood platelets contribution to innate host defense – What they have learned from their big brothers , 2009, Biotechnology journal.

[19]  S. Israels,et al.  Beyond hemostasis: the role of platelets in inflammation, malignancy and infection. , 2008, Cardiovascular & hematological disorders drug targets.

[20]  P. Kubes,et al.  Platelets, neutrophils, and neutrophil extracellular traps (NETs) in sepsis , 2008, Journal of thrombosis and haemostasis : JTH.

[21]  T. Foster,et al.  Molecular Basis for Staphylococcus aureus–Mediated Platelet Aggregate Formation Under Arterial Shear In Vitro , 2007, Arteriosclerosis, thrombosis, and vascular biology.

[22]  T. Foster,et al.  Both Complement- and Fibrinogen-Dependent Mechanisms Contribute to Platelet Aggregation Mediated by Staphylococcus aureus Clumping Factor B , 2007, Infection and Immunity.

[23]  K. Ley,et al.  Platelet-neutrophil-interactions: linking hemostasis and inflammation. , 2007, Blood reviews.

[24]  M. Klouche Diagnostic Methods for Platelet Function Analysis , 2007, Transfusion Medicine and Hemotherapy.

[25]  I. B. Ivanov,et al.  Staphylococcal secretory inhibitor of platelet microbicidal protein is associated with prostatitis source. , 2006, Journal of medical microbiology.

[26]  Niraj Procopio Evagrio George,et al.  Staphylococcus aureus Adhesion via Spa, ClfA, and SdrCDE to Immobilized Platelets Demonstrates Shear-Dependent Behavior , 2006, Arteriosclerosis, thrombosis, and vascular biology.

[27]  Timothy J. Foster,et al.  The interaction of bacterial pathogens with platelets , 2006, Nature Reviews Microbiology.

[28]  Y. Que,et al.  New concepts in the pathophysiology of infective endocarditis , 2006, Current infectious disease reports.

[29]  B. Sinha,et al.  Mechanism and consequences of invasion of endothelial cells by Staphylococcus aureus , 2005, Thrombosis and Haemostasis.

[30]  K. Preissner,et al.  Staphylococcus aureus interactions with the endothelium , 2005, Thrombosis and Haemostasis.

[31]  P. Okoński,et al.  Infekcyjne zapalenie wsierdzia – aktualny stan wiedzy , 2005 .

[32]  A. Bayer,et al.  Beneficial Influence of Platelets on Antibiotic Efficacy in an In Vitro Model of Staphylococcus aureus-Induced Endocarditis , 2004, Antimicrobial Agents and Chemotherapy.

[33]  A. Weyrich,et al.  The evolving role of platelets in inflammation , 2003, Journal of thrombosis and haemostasis : JTH.

[34]  J. Freedman,et al.  Platelets in hemostasis and thrombosis: role of integrins and their ligands. , 2003, Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis.

[35]  J. Vincent,et al.  Platelet function in sepsis , 2002, Journal of thrombosis and haemostasis : JTH.

[36]  A. Cheung,et al.  Clumping Factor A Mediates Binding ofStaphylococcus aureus to Human Platelets , 2001, Infection and Immunity.

[37]  A. Bayer,et al.  Thrombin-Induced Platelet Microbicidal Protein Susceptibility Phenotype Influences the Outcome of Oxacillin Prophylaxis and Therapy of Experimental Staphylococcus aureus Endocarditis , 2000, Antimicrobial Agents and Chemotherapy.

[38]  E. Peerschke,et al.  Staphylococcus aureus Protein A Recognizes Platelet gC1qR/p33: a Novel Mechanism for Staphylococcal Interactions with Platelets , 2000, Infection and Immunity.

[39]  Paul Martin,et al.  Wound Healing--Aiming for Perfect Skin Regeneration , 1997, Science.

[40]  P. Dazin,et al.  Platelet microbicidal protein alone and in combination with antibiotics reduces Staphylococcus aureus adherence to platelets in vitro , 1994, Infection and immunity.

[41]  T. Kiss,et al.  Platelet aggregation in severe sepsis , 2010, Journal of Thrombosis and Thrombolysis.

[42]  I. B. Ivanov,et al.  Assessment of a microplate method for detection of staphylococcal secretory inhibitor of platelet microbicidal protein. , 2009, Diagnostic microbiology and infectious disease.

[43]  R. Diegelmann,et al.  Wound healing: an overview of acute, fibrotic and delayed healing. , 2004, Frontiers in bioscience : a journal and virtual library.

[44]  W. Aird,et al.  Platelet-endothelial interactions: sepsis, HIT, and antiphospholipid syndrome. , 2003, Hematology. American Society of Hematology. Education Program.