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Platelet Inflammatory Response to Stress.
Front Immunol 2019; 10:1478FI

Abstract

Blood platelets play a central hemostatic role, (i) as they repair vascular epithelial damage, and (ii) they play immune defense roles, as they have the capacity to produce and secrete various cytokines, chemokines, and related products. Platelets sense and respond to local dangers (infectious or not). Platelets, therefore, mediate inflammation, express and use receptors to bind infectious pathogen moieties and endogenous ligands, among other components. Platelets contribute to effective pathogen clearance. Damage-associated molecular patterns (DAMPs) are danger signals released during inflammatory stress, such as burns, trauma and infection. Each pathogen is recognized by its specific molecular signature or pathogen-associated molecular pattern (PAMP). Recent data demonstrate that platelets have the capacity to sense external danger signals (DAMPs or PAMPs) differentially through a distinct type of pathogen recognition receptor (such as Toll-like receptors). Platelets regulate the innate immune response to pathogens and/or endogenous molecules, presenting several types of "danger" signals using a complete signalosome. Platelets, therefore, use complex tools to mediate a wide range of functions from danger sensing to tissue repair. Moreover, we noted that the secretory capacity of stored platelets over time and the development of stress lesions by platelets upon collection, processing, and storage are considered stress signals. The key message of this review is the "inflammatory response to stress" function of platelets in an infectious or non-infectious context.

Authors+Show Affiliations

Etablissement Français du Sang Auvergne-Rhône-Alpes, Saint-Étienne, France. GIMAP-EA3064, Université de Lyon, Saint-Étienne, France.Etablissement Français du Sang Auvergne-Rhône-Alpes, Saint-Étienne, France. GIMAP-EA3064, Université de Lyon, Saint-Étienne, France.GIMAP-EA3064, Université de Lyon, Saint-Étienne, France. Laboratoire des Agents Infectieux et d'Hygiène, CHU de Saint-Etienne, Saint-Étienne, France.GIMAP-EA3064, Université de Lyon, Saint-Étienne, France. Laboratoire des Agents Infectieux et d'Hygiène, CHU de Saint-Etienne, Saint-Étienne, France.SAINBIOSE, INSERM U1059, University of Lyon, Saint-Étienne, France. Department of Rheumatology, University Hospital of Saint-Etienne, Saint-Étienne, France.SAINBIOSE, INSERM U1059, University of Lyon, Saint-Étienne, France. Vascular and Therapeutic Medicine Department, Saint-Etienne University Hospital Center, Saint-Étienne, France.GIMAP-EA3064, Université de Lyon, Saint-Étienne, France. Institut National de Transfusion Sanguine, Paris, France.GIMAP-EA3064, Université de Lyon, Saint-Étienne, France.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

31316518

Citation

Cognasse, Fabrice, et al. "Platelet Inflammatory Response to Stress." Frontiers in Immunology, vol. 10, 2019, p. 1478.
Cognasse F, Laradi S, Berthelot P, et al. Platelet Inflammatory Response to Stress. Front Immunol. 2019;10:1478.
Cognasse, F., Laradi, S., Berthelot, P., Bourlet, T., Marotte, H., Mismetti, P., ... Hamzeh-Cognasse, H. (2019). Platelet Inflammatory Response to Stress. Frontiers in Immunology, 10, p. 1478. doi:10.3389/fimmu.2019.01478.
Cognasse F, et al. Platelet Inflammatory Response to Stress. Front Immunol. 2019;10:1478. PubMed PMID: 31316518.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Platelet Inflammatory Response to Stress. AU - Cognasse,Fabrice, AU - Laradi,Sandrine, AU - Berthelot,Philippe, AU - Bourlet,Thomas, AU - Marotte,Hubert, AU - Mismetti,Patrick, AU - Garraud,Olivier, AU - Hamzeh-Cognasse,Hind, Y1 - 2019/06/28/ PY - 2019/03/14/received PY - 2019/06/13/accepted PY - 2019/7/19/entrez PY - 2019/7/19/pubmed PY - 2019/7/19/medline KW - cytokine/chemokine KW - inflammation KW - innate immunity KW - platelets KW - transfusion SP - 1478 EP - 1478 JF - Frontiers in immunology JO - Front Immunol VL - 10 N2 - Blood platelets play a central hemostatic role, (i) as they repair vascular epithelial damage, and (ii) they play immune defense roles, as they have the capacity to produce and secrete various cytokines, chemokines, and related products. Platelets sense and respond to local dangers (infectious or not). Platelets, therefore, mediate inflammation, express and use receptors to bind infectious pathogen moieties and endogenous ligands, among other components. Platelets contribute to effective pathogen clearance. Damage-associated molecular patterns (DAMPs) are danger signals released during inflammatory stress, such as burns, trauma and infection. Each pathogen is recognized by its specific molecular signature or pathogen-associated molecular pattern (PAMP). Recent data demonstrate that platelets have the capacity to sense external danger signals (DAMPs or PAMPs) differentially through a distinct type of pathogen recognition receptor (such as Toll-like receptors). Platelets regulate the innate immune response to pathogens and/or endogenous molecules, presenting several types of "danger" signals using a complete signalosome. Platelets, therefore, use complex tools to mediate a wide range of functions from danger sensing to tissue repair. Moreover, we noted that the secretory capacity of stored platelets over time and the development of stress lesions by platelets upon collection, processing, and storage are considered stress signals. The key message of this review is the "inflammatory response to stress" function of platelets in an infectious or non-infectious context. SN - 1664-3224 UR - https://www.unboundmedicine.com/medline/citation/31316518/Platelet_Inflammatory_Response_to_Stress L2 - https://dx.doi.org/10.3389/fimmu.2019.01478 DB - PRIME DP - Unbound Medicine ER -