The role of blood platelets in infections

COMMENTARY ON THE LAW

The role of blood platelets in infections

Bartłomiej Micota 1 , Beata Sadowska 1 , Barbara Różalska 1

1. Katedra Immunologii i Biologii Infekcyjnej, Uniwersytet Łódzki

Published: 2015-05-17
GICID: 01.3001.0009.6536
Available language versions: en pl
Issue: Postepy Hig Med Dosw 2015; 69 : 624-632

 

Abstract

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.

References

  • 1. Antczak A.J., Vieth J.A., Singh N., Worth R.G.: Internalizationof IgG-coated targets results in activation and secretion of solubleCD40 ligand and RANTES by human platelets. Clin. Vaccine Immunol.,2011; 18: 210-206
    Google Scholar
  • 2. Banach M., Ostrowski S., Okoński P.: Infekcyjne zapalenie wsierdzia– aktualny stan wiedzy. Przew. Lek., 2004; 10: 80-88
    Google Scholar
  • 3. Blair P., Flaumenhaft R.: Platelet α-granules: Basic biology andclinical correlates. Blood Rev., 2009; 23: 177-189
    Google Scholar
  • 4. Chavakis T., Wiechmann K., Preissner K.T., Herrmann M.: Staphylococcusaureus interactions with the endothelium: the role of bacterial“secretable expanded repertoire adhesive molecules” (SERAM) indisturbing host defense systems. Thromb. Haemost., 2005; 94: 278-285
    Google Scholar
  • 5. Cox D., Kerrigan S.W., Watson S.P.: Platelets and the innate immunesystem: mechanisms of bacterial-induced platelet activation.J. Thromb. Haemost., 2011; 9: 1097-1107
    Google Scholar
  • 6. Daga S., Shepherd J.G., Callaghan J.G., Hung R.K., Dawson D.K.,Padfield G.J., Hey S.Y., Cartwright R.A., Newby D.E., Fitzgerald J.R.:Platelet receptor polymorphisms do not influence Staphylococcusaureus – platelet interactions or infective endocarditis. MicrobesInfect., 2011; 13: 216-225
    Google Scholar
  • 7. Dhawan V.K., Bayer A.S., Yeaman M.R.: Thrombin-induced plateletmicrobicidal protein susceptibility phenotype influences the outcomeof oxacillin prophylaxis and therapy of experimental Staphylococcusaureus endocarditis. Antimicrob. Agents Chemother., 2000;44: 3206-3209
    Google Scholar
  • 8. Diegelmann R.F., Evans M.C.: Wound healing: an overview ofacute, fibrotic and delayed healing. Front. Biosci., 2004; 9: 283-289
    Google Scholar
  • 9. Fitzgerald J.R., Foster T.J., Cox D.: The interaction of bacterialpathogens with platelets. Na. Rev. Microbiol., 2006; 4: 445-457
    Google Scholar
  • 10. Garraud O., Berthet J., Hamzeh-Cognasse H., Cognasse F.: Pathogensensing, subsequent signalling, and signalosome in human platelets.Thromb. Res., 2011; 127: 283-286
    Google Scholar
  • 11. George N.P., Wei Q., Shin P.K., Konstantopoulos K., Ross J.M.:Staphylococcus aureus adhesion via Spa, ClfA, and SdrCDE to immobilizedplatelets demonstrates shear-dependent behavior. Arterioscler.Thromb. Vasc. Biol., 2006; 26: 2394-2400
    Google Scholar
  • 12. Grabowski M., Jaworska-Wilczyńska M., Ablewska U., Czerwiń-ska-Jelonkiewicz K., Abramczuk E., Miłkowska M., Hryniewiecki T.:PiśmiennictwoZatorowość ośrodkowego układu nerwowego jako powikłanie infekcyjnegozapalenia wsierdzia. Neurologia i Neurochirurgia Polska,2013; 47: 53-62
    Google Scholar
  • 13. Harding M., Kubes P.: Innate immunity in the vasculature: interactionswith pathogenic bacteria. Curr. Opin. Microbiol., 2012;15: 85-91
    Google Scholar
  • 14. Hryniewiecki T.: Leczenie infekcyjnego zapalenia wsierdzia – cozalecają standardy? Zakażenia, 2007; 1: 29-33
    Google Scholar
  • 15. Ivanov I.B., Gritsenko V.A.: Assessment of a microplate methodfor detection of staphylococcal secretory inhibitor of plateletmicrobicidal protein. Diagn. Microbiol. Infect. Dis., 2009; 63:118-120
    Google Scholar
  • 16. Ivanov I.B., Gritsenko V.A., Kuzmin M.D.: Staphylococcal secretoryinhibitor of platelet microbicidal protein is associated withprostatitis source. J. Med. Microbiol., 2006; 55: 1645-1648
    Google Scholar
  • 17. Johansson D., Shannon O., Rasmussen M.: Platelet and neutrophilresponses to Gram positive pathogens in patients with bacteremicinfection. PLoS One, 2011; 6: e26928
    Google Scholar
  • 18. Kerrigan S.W., Clarke N., Loughman A., Meade G., Foster T.J.,Cox D.: Molecular basis for Staphylococcus aureus – mediated plateletaggregate formation under arterial shear in vitro. Arterioscler.Thromb. Vasc. Biol., 2008; 28: 335-340
    Google Scholar
  • 19. Kerrigan S.W., Cox D.: Platelet–bacterial interactions. Cell. Mol.Life Sci., 2010; 67: 513-523
    Google Scholar
  • 20. Kim H.K., Thammavongsa V., Schneewind O., Missiakas D.: Recurrentinfections and immune evasion strategies of Staphylococcusaureus. Curr. Opin. Microbiol., 2012; 15: 92-99
    Google Scholar
  • 21. Klouche M.: Diagnostic methods for platelet function analysis.Transf. Med. Chemother., 2007; 34: 20-32
    Google Scholar
  • 22. Lacci K.M., Dardik A.: Platelet-rich plasma: support for its usein wound healing. Yale J. Biol. Med. 2010; 83: 1-9
    Google Scholar
  • 23. Łopaciuk U., Tukendorf A.: Infekcyjne zapalenie wsierdzia –czynniki etiologiczne i diagnostyka mikrobiologiczna. AktualnościbioMérieux, 2010; 55: 10-12
    Google Scholar
  • 24. Łuksza E., Mantur M.: Nowe spojrzenie na płytki krwi i mikropłytkiz uwzględnieniem ich roli w zaburzeniach krzepnięcia i progresjichoroby nowotworowej. Pol. Merk. Lek., 2009; 162: 491-495
    Google Scholar
  • 25. Ma A.C., Kubes P.: Platelets, neutrophils, and neutrophil extracellulartraps (NETs) in sepsis. J. Thromb. Haemost., 2008; 6: 415-420
    Google Scholar
  • 26. Mallefet P., Dweck A.C.: Mechanisms involved in wound healing.Biomed. Scientist, 2008; 52: 609-615
    Google Scholar
  • 27. Martin P.: Wound healing-aiming for perfect skin regeneration.Science, 1997; 276: 75-81
    Google Scholar
  • 28. McAdow M., Kim H.K., Dedent A.C., Hendrickx A.P., SchneewindO., Missiakas D.M.: Preventing Staphylococcus aureus sepsis through theinhibition of its agglutination in blood. PLoS Pathog., 2011; 7: e1002307
    Google Scholar
  • 29. McNicol A., Israels, S.J.: Beyond hemostasis: the role of plateletsin inflammation, malignancy and infection. Cardiovasc. Hematol.Disord. Drug Targets, 2008; 8: 99-117
    Google Scholar
  • 30. Mercier R.C., Dietz R.M., Mazzola J.L., Bayer A.S., Yeaman M.R.:Beneficial influence of platelets on antibiotic efficacy in an in vitromodel of Staphylococcus aureus-induced endocarditis. Antimicrob.Agents Chemother., 2004; 48: 2551-2557
    Google Scholar
  • 31. Miajlovic H., Loughman A., Brennan M., Cox D., Foster T.J.: Bothcomplement- and fibrinogen-dependent mechanisms contribute toplatelet aggregation mediated by Staphylococcus aureus clumpingfactor B. Infect. Immun., 2007; 75: 3335-3343
    Google Scholar
  • 32. Moise P.A., Forrest A., Bayer A.S., Xiong Y.Q., Yeaman M.R.,Sakoulas G.: Factors influencing time to vancomycin-induced clearanceof nonendocarditis methicillin-resistant Staphylococcus aureusbacteremia: role of platelet microbicidal protein killing and agr genotypes.J. Infect. Dis., 2010; 15: 233-240
    Google Scholar
  • 33. Nguyen T., Ghebrehiwet B., Peerschke E.I.: Staphylococcus aureusprotein A recognizes platelet gC1qR/p33: a novel mechanism forstaphylococcal interactions with platelets. Infect. Immun., 2000;68: 2061-2068
    Google Scholar
  • 34. Ni H., Freedman J.: Platelets in hemostasis and thrombosis:role of integrins and their ligands. Transf. Apheresis Sci., 2003; 28:257-264
    Google Scholar
  • 35. Polek A., Sobiczewski W., Matowicka-Karna J.: P-selektyna i jejrola w niektórych chorobach. Postępy Hig. Med. Dośw., 2009; 63:465-470
    Google Scholar
  • 36. Rasmussen M., Johansson D., Söbirk S.K., Mörgelin M., ShannonO.: Clinical isolates of Enterococcus faecalis aggregate human platelets.Microb. Infect., 2010; 12: 295-301
    Google Scholar
  • 37. Różalski M.I., Micota B., Sadowska B., Paszkiewicz M.,Więckowska-Szakiel M., Różalska B.: Antimicrobial and anti-biofilmactivity of expired blood platelets and their released products.Postępy Hig. Med. Dośw. 2013; 67: 321-325
    Google Scholar
  • 38. Schubert S., Schwertz, H., Weyrich A.S., Franks Z.G., LindemannS., Otto M.; Behr H., Loppnow H., Schlitt A., Russ M., Presek P., WerdanK., Buerke M.: Staphylococcus aureus α-toxin triggers the synthesisof B-cell lymphoma 3 by human platelets. Toxins, 2011; 3: 120-133
    Google Scholar
  • 39. Shaw T.J., Martin P.: Wound repair at a glance. J. Cell Sci., 2009;122: 3209-3213
    Google Scholar
  • 40. Siboo I.R., Cheung A.L., Bayer A.S., Sullam P.M.: Clumping factorA mediates binding of Staphylococcus aureus to human platelets.Infect. Immun., 2001; 69: 3120-3127
    Google Scholar
  • 41. Sinha B., Herrmann M.: Mechanism and consequences of invasionof endothelial cells by Staphylococcus aureus. Thromb. Haemost.,2005; 94: 266-277
    Google Scholar
  • 42. Warkentin T.E., Aird W.C., Rand J.H.: Platelet-endothelial interactions:sepsis, HIT, and antiphospholipid syndrome. Hematol. Am.Soc. Hematol. Educ. Program, 2003; 1: 497-519
    Google Scholar
  • 43. Ważna E.: Płytki krwi jako regulatory procesów odpornościowych.Postępy Hig. Med. Dośw., 2006; 60: 265-277
    Google Scholar
  • 44. Weyrich A. S., Lindemann, S., Zimmerman G.A.: The evolving roleof platelets in inflammation. J. Thromb. Haemost., 2003; 1: 1897-1905
    Google Scholar
  • 45. Widmer E., Que Y.A., Entenza J.M., Moreillon P.: New conceptsin the pathophysiology of infective endocarditis. Curr. Infect. Dis.Rep., 2006; 8: 271-279
    Google Scholar
  • 46. Woth G., Varga A., Ghosh S., Krupp M., Kiss T., Bogár L., MühlD.: Platelet aggregation in severe sepsis. J. Thromb. Thrombolysis.,2011; 31: 6-12
    Google Scholar
  • 47. Wu B.Q., Zhi M.J., Liu H, Huang J., Zhou Y.Q., Zhang T.T.: Inhibitory effectsof lipoteichoic acid from Staphylococcus aureus on platelet functionand platelet-monocyte aggregation. Inflamm. Res., 2011; 60: 775-782
    Google Scholar
  • 48. Yaguchi A., Lobo F.L., Vincent, J.L., Pradier O.: Platelet functionin sepsis. J. Thromb. Haemost., 2004; 2: 2096-2102
    Google Scholar
  • 49. Yeaman M.R.: Platelets in defense against bacterial pathogens.Cell. Mol. Life Sci., 2010; 67: 525-544
    Google Scholar
  • 50. Yeaman M.R., Sullam P.M., Dazin P.F., Bayer A.S.: Platelet microbicidalprotein alone and in combination with antibiotics reducesStaphylococcus aureus adherence to platelets in vitro. Infect. Immun.,1994; 62: 3416-3423
    Google Scholar
  • 51. Zander D.M., Klinger M.: The blood platelets contribution to innatehost defense – what they have learned from their big brothers.Biotechnol. J., 2009; 4: 914-926
    Google Scholar
  • 52. Zarbock A., Polanowska-Grabowska R.K., Ley K.: Platelet-neutrophil-interactions:Linking hemostasis and inflammation. BloodRev., 2007; 21: 99-111
    Google Scholar

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