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4 - Platelet priming
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- By Emanuela Falcinelli, Stefania Momi, Division of Internal and Cardiovascular Medicine, Department of Internal Medicine, University of Perugia, Perugia, Italy
- Edited by Paolo Gresele, Università degli Studi di Perugia, Italy, Valentin Fuster, Mount Sinai School of Medicine, New York, Jose A. Lopez, Seattle University, Clive P. Page, King's College London, Jos Vermylen, Katholieke Universiteit Leuven, Belgium
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- Book:
- Platelets in Hematologic and Cardiovascular Disorders
- Published online:
- 15 October 2009
- Print publication:
- 13 December 2007, pp 53-78
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Summary
INTRODUCTION
One of the regulatory mechanisms controlling the response of excitable cells to stimuli is priming. The term “priming” is used when the prior exposure to a given mediator predisposes a cell to a more effective response to a subsequent stimulus.
Priming has been described for cells as disparate as the neutrophil and myocyte. The initial stimulus (primer) transmits a message to the intracellular signaling machinery that influences the cell's response to a subsequent challenge. This may result, for instance, in an exaggerated inflammatory response in the case of the neutrophil or in an improved tolerance to injury for the myocyte. Neutrophil priming, by agents like tumor necrosis factor alpha (TNF-α), lipopolysac-charide (LPS) and granulocyte/macrophage colony-stimulating factor (GM-CSF), causes a dramatic increase in the capacity to induce tissue injury in response to a subsequent stimulus. This is achieved by the enhancement of superoxide anion generation, degranulation and lipid mediator release. Whereas different cells respond differently to priming stimuli, the intracellular targets appear to be similar; for instance, the priming of both neutrophils and myocytes involves protein kinase C (PKC) activation (although the PKC isoform profile is stimulus-specific and determines the specific functional response of the cell). Recent studies support a key role also for protein tyrosine phosphorylation and enhanced phospholipase D and phosphoinositide 3-kinase-gamma (PI3K-γ) activation in neutrophil priming.
19 - Platelets in respiratory disorders and inflammatory conditions
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- By Stefania Momi, Department of Internal Medicine, University of Perugia, Italy, Simon C. Pitchford, National Heart and Lung Institute, Imperial College London, UK
- Edited by Paolo Gresele, Università degli Studi di Perugia, Italy, Valentin Fuster, Mount Sinai School of Medicine, New York, Jose A. Lopez, Seattle University, Clive P. Page, King's College London, Jos Vermylen, Katholieke Universiteit Leuven, Belgium
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- Book:
- Platelets in Hematologic and Cardiovascular Disorders
- Published online:
- 15 October 2009
- Print publication:
- 13 December 2007, pp 323-340
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Summary
INTRODUCTION
Over the last years increasing attention has been directed to the previously unrecognized role of platelets in inflammatory processes, including atherogenesis, ischemia–reperfusion injury, and sepsis.
Several studies have revealed alterations of platelets from patients with inflammatory diseases, and these alterations have been dissociated from the well-characterized involvement of platelets in thrombosis and hemostasis. The mechanisms by which platelets participate in inflammation are still being discovered, but there is now wider acceptance that platelets act as innate inflammatory cells in the immune response with roles as sentinel cells exerting surveillance and responding to microbial invasion, tissue damage, and antigen challenge. Platelet activation by proinflammatory mediators, functional interactions with other cells involved in inflammation, and the evidence that platelets undergo chemotaxis through inflamed tissue are testimony that platelets directly participate in inflammation. Platelets appear to be involved in the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic infections, allergic inflammation (including asthma and rhinitis), chronic obstructive pulmonary disease (COPD), cystic fibrosis, rheumatoid arthritis (RA), allergic dermatologic disorders, and inflammatory bowel diseases. Platelets also play a role as inflammatory cells in atherogenesis, a topic discussed in Chapter. The aim of this chapter is to give an overview on the role of platelets in inflammation, starting from the structural, biochemical, and functional properties that characterize platelets as inflammatory cells, and then to discuss their participation in some inflammatory disorders with evidence derived from experimental studies in animals and from observations in patients.
27 - Platelets and chemotaxis
- from PART I - PHYSIOLOGY
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- By Stefania Momi, Division of Internal and Cardiovascular Medicine, Department of Internal Medicine, University of Perugia, Italy, Paolo Gresele, Division of Internal and Cardiovascular Medicine, Department of Internal Medicine, University of Perugia, Italy
- Edited by Paolo Gresele, Università degli Studi di Perugia, Italy, Clive P. Page, Valentin Fuster, Jos Vermylen, Universiteitsbibliotheek-K.U., Leuven
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- Book:
- Platelets in Thrombotic and Non-Thrombotic Disorders
- Published online:
- 10 May 2010
- Print publication:
- 30 May 2002, pp 393-411
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Summary
Introduction
Platelets have been considered mostly for their role in hemostasis, thrombosis and vascular disease; however, many studies over the last few decades have provided an emerging body of evidence on their potential role in host defence reactions. This unconventional function of platelets is consistent with the theory that platelets may represent the phylogenetic vestige of the primitive hemocytes of lower organisms. As hemocytes, which exert a central role both in defence against invading microorganisms and in repair of tissue injury, platelets maintain in many regards the function of inflammatory cells, able to activate complement, secrete proteases, alter vascular permeability and tone and express cytotoxic properties. For instance, platelets have been shown to participate in cytotoxicity against the parasites responsible for shistosomiasis, toxoplasmosis, and trypanosomiasis.
Although platelets are anucleated cells, they have an anatomical structure and biochemical properties in many aspects similar to leukocytes and it is thus conceivable that platelets may participate in the defence against infections and in other inflammatory responses. For instance, several observations have confirmed the involvement of platelets in allergic disease and in particular in the tissue inflammatory changes associated with allergic asthma. However, given the role of paramount importance that platelets play in hemostasis and thrombosis and considering the complicacy of the mechanisms regulating these functions, which have absorbed much of the research efforts on these cells, little attention has been paid to the mechanisms regulating platelet inflammatory activities. This chapter will discuss functional activities of platelets related to chemotaxis, an important step in cell involvement in tissue inflammation.