Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antoantibodies to cholesterol were detected and purified from normal (nonimmunized) pig serum. The antibodies were assayed by ELISA with crystalline cholesterol as an Ag and by C-dependent damage to cholesterol-laden liposomes. Intravenous injection of liposomes containing cholesterol into anesthetized animals caused decreased hemolytic complement titers, and induced a reaction consisting of transient neutropenia, thrombocytopenia, respiratory distress, cyanosis, pulmonary and systemic hypertension, and decreased cardiac output. Plasma levels of thromboxane B2 and 6-keto-prostaglandin F1 alpha increased 1300 and 200%, respectively, and leukocyte and platelet counts decreased by 36 and 38%, respectively. Injection of cholesterol-free liposomes did not induce the reaction. These results show that naturally occurring autoantibodies to cholesterol can initiate C activation and can be associated with anaphylactoid reaction to exogenously administered cholesterol in pigs.
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PMID:Anaphylactoid reactions mediated by autoantibodies to cholesterol in miniature pigs. 280 13

Administration of the mucopolysaccharide, carrageenan (CAR), into the hind paw of the rat or mouse induces a local inflammation characterized by increased arachidonic acid metabolism, increased vascular permeability, edema, and neutrophil extravasation. Carrageenan-induced hind-paw inflammation is inhibited by prostaglandin synthesis inhibitors, and this assay predicts the clinical success of anti-inflammatory agents in reducing peripheral inflammation. The purpose of this study was to determine if intraventricular injection of CAR would induce brain inflammation similar to that evoked by CAR in peripheral tissues. The present study demonstrates that CAR injection into the ventricles of the mouse brain does in fact induce an inflammatory response very similar to that caused by injection of CAR into the peripheral tissues. The brain response to CAR was dose-dependent, with the maximum increase in cerebrovascular permeability to iodine-125-labeled human serum albumin and percent brain water occurring after injection of 50 micrograms CAR. As is seen in CAR-induced inflammation of the hind paw, the maximum increase in brain vascular permeability occurred 4 hours after CAR injection. Histological analysis of brains 4 hours after CAR administration showed global neutrophil extravasation into the subarachnoid space and evidence of focal neuronal swelling. Methotrexate-induced neutropenia, however, failed to diminish the permeability response to CAR. Gas chromatographic and mass spectrometric measurements of brain prostaglandins 4 hours after CAR injection revealed a significantly increased level of 6-keto-prostaglandin F1 alpha. These results indicate that a significant increase in prostacyclin, the pro-inflammatory arachidonic acid metabolite, during CAR-induced brain inflammation is likely. These studies suggest that CAR-induced brain inflammation may be a useful model on which to test the efficacy of anti-inflammatory agents in the brain, as well as providing information concerning the mediators and mechanisms by which the brain may sustain inflammatory injury.
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PMID:Carrageenan-induced brain inflammation. Characterization of the model. 377 56