Gut
Serotonin is produced and released for platelet uptake.
Animals—including humans—cannot make tryptophan, the precursor of serotonin, but have to ingest it with plant food.
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CD62P is an activation marker.
In resting platelets CD62P is part of the α-granule membrane.
During activation and α-granule release it appears on the cell surface.
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An imbalance of bacterial species in the intestines is called dysbiosis.
Dysbiosis can follow antibiotic treatment.
Dysbiosis is associated with low serotonin production.
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Enterochromaffin cells in the intestinal wall are specialized in serotonin production.
The aminoacid tryptophan is the precursor of serotonin, 5‐hydroxytryptamine or 5‐HT.
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Expression of FcγRII on the surface of activated platelets is part of the innate immune response.
FCγRII signals to macrophages that the platelet should be removed.
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Serotonin is one of the chemicals that keep the gut wall tight.
With dysbiosis and serotonin deficiency gaps in the intestinal lining cause leaky gut.
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Microbiota refers to all bacteria, viruses and yeasts living in the intestines.
Microbes inform the immune system.
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When platelets activate they shed microparticles (MP).
Microparticles communicate with other parts of the body.
Example: MP shed by tumor-informed platelets are associated with metastases.
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Platelets are innate immune cells.
Platelets are the first line of defense against foreign substances in the blood.
Platelets communicate through the changes occurring during activation.
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Soluble CD40L is released during platelet activation.
High plasma sCD40L is an indicator of inflammation.
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Some gut microbes produce serotonin.
Others stimulate enterochromaffin cells to produce and release it.
Platelets take up serotonin mostly through the serotonin transporter (SERT).
Selective serotonin reuptake inhibitors (SSRIs) block serotonin uptake.
SSRIs affect platelets and their function.