Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously described the appearance in serum of increased neutrophil chemotactic activity (NCA) during bronchospasm induced by inhalation of ragweed antigen in ragweed-sensitive subjects. This NCA is non-complement derived, appears within 1 min after antigen inhalation, and is not seen after methacholine-induced bronchospasm. This article describes further characterization of this chemotactic activity and correlation with in vivo leukocytosis. NCA consistently eluted in the void volume (fraction I) after Sephadex G-150 chromatography of patient serum obtained 10 min postchallenge. Fraction I contained 94% of the NCA of postchallenge whole serum. Both postchallenge whole serum and fraction I deactivated neutrophils to autologous chemoattractants and complement-derived chemotactic factors, but not serum-independent chemotactic factors. NCA was chemotactic for neither human nor guinea pig eosinophils, nor for human mononuclear cells. A significant increase of circulating neutrophils was seen only after antigen-induced bronchospasm and correlated with the increase in NCA. Thus, NCA represents another inflammatory mediator of probable mast cell origin that may explain, at least partially, the accumulation of neutrophils observed in the peripheral blood, skin, and bronchial wall after immediate hypersensitivity reactions.
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PMID:Further characterization and biologic activity of ragweed antigen--induced neutrophil chemotactic activity in man. 47 76

When the tridecamer component of compound 48/80 (Fraction D, Fr.D), a Ca2+-dependent histamine releaser, was incubated with rat mast cells that had been prelabeled with [32P]phosphate, [3H]inositol or [3H]glycerol, it induced a rapid decrease in [32P]phosphatidylinositol-4,5-bisphosphate (PIP2) followed by increases of [3H]inositol-1,4,5-trisphosphate (Ins P3) and [3H]diacylglycerol during the 10 sec prior to detectable histamine release. Fr.D-induced changes of the metabolism of these compounds occurred even in the absence of Ca2+, but to a lesser extent than in the presence of Ca2+. In contrast, the accumulation of [3H]arachidonic acid into phosphatidylcholine (PC), phosphatidylinositol (PI) and phosphatidic acid (PA) in [3H]arachidonic acid-prelabeled mast cells was Ca2+-dependently stimulated by Fr.D with a concomitant decrease in [3H]phosphatidylethanolamine (PE). These Ca2+-dependent changes in PC and PE were not observed in mast cells preloaded with [32P]phosphate, while [32P]PI and [32P]PA increased Ca2+ independently. Fr.D also increased 45Ca2+ uptake by mast cells within 5 sec after the stimulation. These results indicate that Fr.D binding to mast cell Ca2+ independently induces rapid changes of PI cycle-related metabolism of plasma membrane components, while it also induces Ca2+-dependent accumulation of arachidonic acid into PC, PI and PA in association with the decrease of PE, which may be important during the latent period prior to the Ca2+-dependent release of histamine from Fr.D-stimulated mast cells.
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PMID:Effect of the tridecamer of compound 48/80, a Ca2+-dependent histamine releaser, on phospholipid metabolism during the early stage of histamine release from rat mast cells. 377 3