Beh Marlin, se è per questo Bizzozzero scoprì H.pilori ben 100 anni fa ma solo negli anni 80 Robin Warren dimostrò che era la principale causa dell'ulcera gastrica. Ora a me viene il dubbio che qualcosa causi o quantomeno PEGGIORI l'infiammazione...
Anche perché H. Pilori è presente in 40% della popolazione ma l'ulcera colpisce una percentuale più bassa. I fattori genetici sono predisponenti ma l'eziologia è in ultima analisi infettiva.
Prostaglandin D2 (or PGD2) is a prostaglandin that binds to the receptor PTGDR, as well as CRTH2.[1][2] It is a major prostaglandin produced by mast cells – recruits Th2 cells, eosinophils, and basophils. In mammalian organs, large amounts of PGD2 are found only in the brain and in mast cells. It is critical to development of allergic diseases such as asthma.
Mast cells express a high-affinity receptor (Fc#949;RI) for the Fc region of IgE, the least-abundant member of the antibodies. This receptor is of such high affinity that binding of IgE molecules is essentially irreversible. As a result, mast cells** are coated with IgE. IgE is produced by plasma cells (the antibody-producing cells of the immune system). IgE molecules, like all antibodies, are specific to one particular antigen.
In allergic reactions, mast cells** remain inactive until an allergen binds to IgE already in association with the cell (see above). Other membrane activation events can either prime mast cells for subsequent degranulation or can act in synergy with FceRI signal transduction.[7] Allergens are generally proteins or polysaccharides. The allergen binds to the antigen-binding sites, which are situated on the variable regions of the IgE molecules bound to the mast cell surface. It appears that binding of two or more IgE molecules (cross-linking) is required to activate the mast cell. The clustering of the intracellular domains of the cell-bound Fc receptors, which are associated with the cross-linked IgE molecules, causes a complex sequence of reactions inside the mast cell that lead to its activation. Although this reaction is most well understood in terms of allergy, it appears to have evolved as a defense system against intestinal worm infestations** (tapeworms, etc.)[citation needed].
The molecules thus released into the extracellular environment include:[2]
preformed mediators (from the granules):
serine proteases, such as tryptase
histamine (2-5 pg/cell)
serotonin
proteoglycans, mainly heparin (active as anticoagulant)
newly formed lipid mediators (eicosanoids):
thromboxane
--> prostaglandin D2
leukotriene C4
platelet-activating factor
cytokines
Eosinophil chemotactic factor
potrebbero (si noti il condizionale) essere in ultima analisi utili gli stessi farmaci impiegati nei disordini autoimmuni e asmatici, tentando di stabilizzare la degranulazione delle mastcellule e dei basofili. le IgE potrebbero essere:
- qualcosa relativo al metabolismo dei parassiti,
- qualcosa di relativo a batteri che parassitano i parassiti (so che può sembrare paradossale)
- cross-reattività?
Ad ogni modo l'associazione di PGD2 e infiltrato basofilo non può essere una coincidenza e forse l'alopecia dovrebbe essere più di pertinenza dell'immunologo che del dermatologo.
Anche perché H. Pilori è presente in 40% della popolazione ma l'ulcera colpisce una percentuale più bassa. I fattori genetici sono predisponenti ma l'eziologia è in ultima analisi infettiva.
Prostaglandin D2 (or PGD2) is a prostaglandin that binds to the receptor PTGDR, as well as CRTH2.[1][2] It is a major prostaglandin produced by mast cells – recruits Th2 cells, eosinophils, and basophils. In mammalian organs, large amounts of PGD2 are found only in the brain and in mast cells. It is critical to development of allergic diseases such as asthma.
Mast cells express a high-affinity receptor (Fc#949;RI) for the Fc region of IgE, the least-abundant member of the antibodies. This receptor is of such high affinity that binding of IgE molecules is essentially irreversible. As a result, mast cells** are coated with IgE. IgE is produced by plasma cells (the antibody-producing cells of the immune system). IgE molecules, like all antibodies, are specific to one particular antigen.
In allergic reactions, mast cells** remain inactive until an allergen binds to IgE already in association with the cell (see above). Other membrane activation events can either prime mast cells for subsequent degranulation or can act in synergy with FceRI signal transduction.[7] Allergens are generally proteins or polysaccharides. The allergen binds to the antigen-binding sites, which are situated on the variable regions of the IgE molecules bound to the mast cell surface. It appears that binding of two or more IgE molecules (cross-linking) is required to activate the mast cell. The clustering of the intracellular domains of the cell-bound Fc receptors, which are associated with the cross-linked IgE molecules, causes a complex sequence of reactions inside the mast cell that lead to its activation. Although this reaction is most well understood in terms of allergy, it appears to have evolved as a defense system against intestinal worm infestations** (tapeworms, etc.)[citation needed].
The molecules thus released into the extracellular environment include:[2]
preformed mediators (from the granules):
serine proteases, such as tryptase
histamine (2-5 pg/cell)
serotonin
proteoglycans, mainly heparin (active as anticoagulant)
newly formed lipid mediators (eicosanoids):
thromboxane
--> prostaglandin D2
leukotriene C4
platelet-activating factor
cytokines
Eosinophil chemotactic factor
potrebbero (si noti il condizionale) essere in ultima analisi utili gli stessi farmaci impiegati nei disordini autoimmuni e asmatici, tentando di stabilizzare la degranulazione delle mastcellule e dei basofili. le IgE potrebbero essere:
- qualcosa relativo al metabolismo dei parassiti,
- qualcosa di relativo a batteri che parassitano i parassiti (so che può sembrare paradossale)
- cross-reattività?
Ad ogni modo l'associazione di PGD2 e infiltrato basofilo non può essere una coincidenza e forse l'alopecia dovrebbe essere più di pertinenza dell'immunologo che del dermatologo.
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