• Toxicofera venom evolution
• coagulation cascade
• hemostasis-affecting toxins
• kallikrein–kinin system
• platelet activation
• snake venom serine protease
• venom toxin

• Animals
• Serine Proteases/metabolism
• Reptiles
• Humans

• FAPDF 193.001.760/2017 Fundação de Apoio à Pesquisa do Distrito Federal

• 28-day mortality
• D-dimer
• biomarkers
• congestive heart failure
• inflammation
• platelet/lymphocyte ratio
• thrombin time

• IgA nephropathy
• chronic kidney disease
• platelet-to-albumin ratio
• platelet-to-lymphocyte ratio
• renal and cardiovascular prognosis

• essential thrombocythemia
• immune thrombocytopenic purpura
• platelet oscillation

• Autoantigens/metabolism
• Cytokines/metabolism
• Genetic Predisposition to Disease
• Humans
• Iodide Peroxidase/metabolism
• Iron-Binding Proteins/metabolism
• Purpura, Thrombocytopenic, Idiopathic/genetics
• Purpura, Thrombocytopenic, Idiopathic/metabolism
• Thrombocythemia, Essential/genetics
• Thrombocythemia, Essential/metabolism

Aging is associated with changes to the immune system, collectively termed immunosenescence and inflammageing. However, the relationships among age, frailty, and immune parameters in older people resident in care homes are not well described. We assessed immune and inflammatory parameters in 184 United Kingdom care home residents aged over 65 years and how they relate to age, frailty index, and length of care home residence. Linear regression was used to identify the independent contribution of age, frailty, and length of care home residence to the various immune parameters as dependent variables. Participants had a mean age (±SD) of 85.3 ± 7.5 years, had been residing in the care home for a mean (±SD) of 1.9 ± 2.2 years at the time of study commencement, and 40.7% were severely frail. Length of care home residence and frailty index were correlated but age and frailty index and age and length of care home residence were not significantly correlated. All components of the full blood count, apart from total lymphocytes, were within the reference range; 31% of participants had blood lymphocyte numbers below the lower value of the reference range. Among the components of the full blood count, platelet numbers were positively associated with frailty index. Amongst plasma inflammatory markers, C-reactive protein (CRP), interleukin-1 receptor antagonist (IL-1ra), soluble E-selectin and interferon gamma-induced protein 10 (IP-10) were positively associated with frailty. Plasma soluble vascular cell adhesion molecule 1 (sVCAM-1), IP-10 and tumor necrosis factor receptor II (TNFRII) were positively associated with age. Plasma monocyte chemoattractant protein 1 was positively associated with length of care home residence. Frailty was an independent predictor of platelet numbers, plasma CRP, IL-1ra, IP-10, and sE-selectin. Age was an independent predictor of activated monocytes and plasma IP-10, TNFRII and sVCAM-1. Length of care home residence was an independent predictor of plasma MCP-1. This study concludes that there are independent links between increased frailty and inflammation and between increased age and inflammation amongst older people resident in care homes in the United Kingdom. Since, inflammation is known to contribute to morbidity and mortality in older people, the causes and consequences of inflammation in this population should be further explored.

• 3D microvessels
• PfEMP1
• Plasmodium falciparum
• blood vessels
• cerebral malaria
• vascular engineering

• Chemokine
• Cytokine
• Hemoglobinopathy
• Sickle-cell disease (SCD)

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.

• cytokine/chemokine
• inflammation
• innate immunity
• platelets
• transfusion

• Adult
• Blood Platelets/metabolism
• Cytokines/genetics
• Cytokines/metabolism
• Embryo Implantation/drug effects
• Endometrium/drug effects
• Endometrium/metabolism
• Female
• Humans
• Intercellular Signaling Peptides and Proteins/metabolism
• Leukocytes, Mononuclear/cytology
• Leukocytes, Mononuclear/metabolism
• Platelet Transfusion
• Platelet-Rich Plasma/cytology
• Platelet-Rich Plasma/metabolism
• Pregnancy
• Reproductive Techniques, Assisted

Platelets are considered as significant players in innate and adaptive immune responses. The adhesion molecules they express, including P-selectin, CD40L, and CD42b, facilitate interactions with many cellular effectors. Upon interacting with a pathogen, platelets rapidly express and enhance their adhesion molecules, and secrete cytokines and chemokines. A similar phenomenon occurs after exposure of platelets to thrombin, an agonist extensively used for in vitro activation of these cells. It was recently reported that the dengue virus not only interacts with platelets but possibly infects them, which triggers an increased expression of adhesion molecule P-selectin as well as secretion of IL-1β. In the present study, surface molecules of platelets like CD40L, CD42b, CD62P, and MHC class I were evaluated at 4 h of interaction with dengue virus serotype 2 (DENV-2), finding that DENV-2 induced a sharp rise in the membrane expression of all these molecules. At 2 and 4 h of DENV-2 stimulation of platelets, a significantly greater secretion of soluble CD40L (sCD40L) was found (versus basal levels) as well as cytokines such as GM-CSF, IL-6, IL-8, IL-10, and TNF-α. Compared to basal, DENV-2 elicited more than two-fold increase in these cytokines. Compared to the thrombin-induced response, the level generated by DENV-2 was much higher for GM-CSF, IL-6, and TNF-α. All these events induced by DENV end up in conspicuous morphological changes observed in platelets by confocal microscopy and transmission electron microscopy, very different from those elicited by thrombin in a more physiological scenery.

• CD40L
• Immune response
• dengue virus
• platelets

Platelets transfusion is a safe process, but during or after the process, the recipient may experience an adverse reaction and occasionally a serious adverse reaction (SAR). In this review, we focus on the inflammatory potential of platelet components (PCs) and their involvement in SARs. Recent evidence has highlighted a central role for platelets in the host inflammatory and immune responses. Blood platelets are involved in inflammation and various other aspects of innate immunity through the release of a plethora of immunomodulatory cytokines, chemokines, and associated molecules, collectively termed biological response modifiers that behave like ligands for endothelial and leukocyte receptors and for platelets themselves. The involvement of PCs in SARs—particularly on a critically ill patient’s context—could be related, at least in part, to the inflammatory functions of platelets, acquired during storage lesions. Moreover, we focus on causal link between platelet activation and immune-mediated disorders (transfusion-associated immunomodulation, platelets, polyanions, and bacterial defense and alloimmunization). This is linked to the platelets’ propensity to be activated even in the absence of deliberate stimuli and to the occurrence of time-dependent storage lesions.

• CD40L
• inflammation
• innate immunity
• platelets
• serious adverse reaction
• transfusion

• Bee venom
• Diabetes
• Healing factors
• Platelets
• Propolis
• Whey proteins
• Wound

• Animals
• Bee Venoms/therapeutic use
• Blood Platelets/immunology
• Humans
• Propolis/therapeutic use
• Whey Proteins/therapeutic use
• Wound Healing/drug effects
• Wound Healing/immunology

• Cytokines
• Primary immune thrombocytopenia
• T helper cells
• Thrombopoietin receptor agonists

• allergic transfusion reactions
• anaphylaxis
• basophil activation test

• Animals
• Biomarkers/blood
• Blood Platelets/immunology
• Blood Platelets/metabolism
• Humans
• Immunomodulation
• Inflammation/blood
• Inflammation/diagnosis
• Inflammation/immunology
• Platelet Activation/immunology

• Allergie
• Allergy
• Antibodies
• Anticorps
• Cytokines
• Hemovigilance
• Hémovigilance
• Inflammation
• TRALI
• Transfusion

• Acute Lung Injury/etiology
• Acute Lung Injury/prevention & control
• Apoptosis
• Blood Cells/immunology
• Blood Preservation
• Blood Transfusion/trends
• Genetic Predisposition to Disease
• Humans
• Hypersensitivity/etiology
• Hypersensitivity/immunology
• Inflammation/etiology
• Inflammation/prevention & control
• Iron/adverse effects
• Iron/blood
• Isoantibodies/blood
• Isoantibodies/immunology
• Leukocyte Reduction Procedures
• Transfusion Reaction/etiology
• Transfusion Reaction/immunology
• Transfusion Reaction/prevention & control

• adhesion
• chemokine
• cytokine
• infection
• inflammation
• platelet
• sepsis

Small fragments circulating in the blood were formally identified by the end of the nineteenth century, and it was suggested that they assisted coagulation via interactions with vessel endothelia. Wright, at the beginning of the twentieth century, identified their bone-marrow origin. For long, platelets have been considered sticky assistants of hemostasis and pollutants of blood or tissue samples; they were just cell fragments. As such, however, they were acknowledged as immunizing (to specific HPA and HLA markers): the platelet’s dark face. The enlightened face showed that besides hemostasis, platelets contained factors involved in healing. As early as 1930s, platelets entered the arsenal of medicines were transfused, and were soon manipulated to become a kind of glue to repair damaged tissues. Some gladly categorized platelets as cells but they were certainly not fully licensed as such for cell physiologists. Actually, platelets possess almost every characteristic of cells, apart from being capable of organizing their genes: they have neither a nucleus nor genes. This view prevailed until it became evident that platelets play a role in homeostasis and interact with cells other than with vascular endothelial cells; then began the era of physiological and also pathological inflammation. Platelets have now entered the field of immunity as inflammatory cells. Does assistance to immune cells itself suffice to license a cell as an “immune cell”? Platelets prove capable of sensing different types of signals and organizing an appropriate response. Many cells can do that. However, platelets can use a complete signalosome (apart from the last transcription step, though it is likely that this step can be circumvented by retrotranscribing RNA messages). The question has also arisen as to whether platelets can present antigen via their abundantly expressed MHC class I molecules. In combination, these properties argue in favor of allowing platelets the title of immune cells.

• cell biology
• cell physiology
• cytokines
• hemostasis
• immunopathology
• immunophysiology
• platelets

• adverse transfusion reaction
• allergic reaction
• first transfusion
• haemovigilance
• transfusion episode

• Adult
• Aged
• Blood Platelets/immunology
• CD40 Ligand/blood
• Chemokine CCL3/blood
• Computer Simulation
• Cytokines/metabolism
• Decision Trees
• Female
• Humans
• Inflammation
• Interleukin-13/blood
• Male
• Middle Aged
• Models, Statistical
• Platelet Transfusion/adverse effects
• Risk
• Young Adult

• haemovigilance
• laboratory test
• nonhaemolytic transfusion reaction

• Acute Lung Injury/etiology
• Acute Lung Injury/immunology
• Apoptosis
• Blood Cells/physiology
• Blood Cells/ultrastructure
• Blood Donors
• Blood Preservation
• Cell-Derived Microparticles
• Cellular Senescence
• Cytokines/blood
• Disease Susceptibility
• Fever/etiology
• Graft vs Host Reaction
• Humans
• Hypersensitivity/etiology
• Immunologic Factors/blood
• Inflammation/etiology
• Inflammation Mediators/blood
• Leukocyte Reduction Procedures
• Leukocytes/immunology
• Reagins/immunology
• Receptors, IgG/blood
• Solutions/adverse effects
• Transfusion Reaction

Non-haemolytic transfusion reactions are the most common type of transfusion reaction and include transfusion-related acute lung injury, transfusion-associated circulatory overload, allergic reactions, febrile reactions, post-transfusion purpura and graft-versus- host disease. Although life-threatening anaphylaxis occurs rarely, allergic reactions occur most frequently. If possible, even mild transfusion reactions should be avoided because they add to patients' existing suffering. During the last decade, several new discoveries have been made in the field of allergic diseases and transfusion medicine. First, mast cells are not the only cells that are key players in allergic diseases, particularly in the murine immune system. Second, it has been suggested that immunologically active undigested or digested food allergens in a donor's blood may be transferred to a recipient who is allergic to these antigens, causing anaphylaxis. Third, washed platelets have been shown to be effective for preventing allergic transfusion reactions, although substantial numbers of platelets are lost during washing procedures, and platelet recovery after transfusion may not be equivalent to that with unwashed platelets. This review describes allergic transfusion reactions, including the above-mentioned points, and focusses on their incidence, pathogenesis, laboratory tests, prevention and treatment.