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At least 883 records · Page 49Linked to original sources
PubMed1991

Structure and biological activities of a new mastoparan isolated from the venom of the hornet Vespa basalis.

By gel filtration on a Fractogel TSK HW 50 column followed by cation-exchange chromatography on CM-Trisacryl M, a tetradecapeptide amide, designated 'mastoparan B', was purified from the venom of the hornet Vespa basalis. Its amino acid sequence was determined as: Leu-Lys-Leu-Lys-Ser-Ile-Val-Ser-Trp-Ala-Lys-Lys-Val-Leu-NH2 and its molecular mass was measured to be 1611 Da by fast-atom-bombardment mass spectrometry. In addition to having a common structure of vespid mastoparans, the peptide shows a less hydrophobic sequence at positions 1, 2, 5, 8 and 9. The peptide caused liberation of histamine from rat peritoneal mast cells and induced oedema in the rat paw. However, the latter effect was inhibited by 'anti-serotonin' (anti-5-hydroxytryptamine) (cyproheptadine), but not by antihistamine (chlorpheniramine). The peptide also possesses a potent haemolytic activity which acts in synergy with the lethal protein of the venom, suggesting the possible involvement of mastoparan B in the lethal effect of Vespa basalis venom.

Amino Acid Sequence↗
PubMed1963

STUDIES ON THE LOCALIZATION OF CIRCULATING ANTIGEN-ANTIBODY COMPLEXES AND OTHER MACROMOLECULES IN VESSELS. II. PATHOGENETIC AND PHARMACODYNAMIC STUDIES.

Localization of circulating antigen-antibody complexes in vessels of guinea pigs by means of anaphylactic shock was found to be mediated by histamine that was released at the time of anaphylaxis. The source of the histamine may have been the mast cell as noted in studies employing a direct attack on the mast cells by octylamine. Platelets played apparently little to no role in guinea pigs in the anaphylactic deposition of circulating complexes. Rat anaphylatoxin was found to cause vascular localization and symptoms of anaphylaxis identical with that brought about by antigen-antibody anaphylaxis. This also was found to be dependent upon the release of histamine. Antibody against Forssman antigen in the vessel walls of the guinea pigs also led to deposition of circulating complexes. This was found not to be histamine dependent. The possible role of local increase in vascular permeability in certain experimental disease states in the localization of circulating complexes is discussed.

Anaphylaxis↗
PubMed1964

A COMPARISON OF THE SPECIFICITY OF INHIBITION BY PHOSPHONATE ESTERS OF THE FIRST COMPONENT OF COMPLEMENT AND THE ANTIGEN-INDUCED RELEASE OF HISTAMINE FROM GUINEA PIG LUNG.

The ability of a number p-nitrophenylethyl alkyl, phenyl alkyl, chloroalkyl, and aminoalkyl phosphonates to inhibit the activated first component (C'1a) of guinea pig complement, and the antigen-induced release of histamine from sliced, perfused guinea pig lung has been compared. C'1a in its reactivity with these phosphonates is distinctly more similar to trypsin than to any of the other enzymes studied previously. It is suggested that both trypsin and C'1a possess an anionic group in the active center of the respective enzyme, but the distance between the anionic and esteratic site in C'1a might be less than in trypsin. The pattern of inhibition of histamine relase by the alkyl, phenyl alkyl, and chloroalkyl phosphonates is similar to the inhibition of C'1a by these compounds, although distinct differences are apparent. The aminoalkyl phosphonates are distinctly less active inhibitors of histamine release than the corresponding alkyl phosphonates, whereas the reverse is true of the inhibition of C'1a. On the basis of these differences, it is tentatively concluded that the organophosphorus-inhibitable enzymes in the guinea pig systems studied here are similar but not identical.

Animals↗
PubMed1964

STUDIES ON THE MECHANISMS OF HYPERSENSITIVITY PHENOMENA. IX. HISTAMINE RELEASE FROM HUMAN LEUKOCYTES BY RAGWEED POLLEN ANTIGEN.

Human leukocytes, isolated from the blood of ragweed-sensitive donors, release histamine upon reaction with a purified protein antigen derived from this pollen. The release process has been studied with washed cells suspended in a defined, serum-free medium. Physiologic levels of pH, ionic strength, and temperature, as well as both calcium and magnesium, are required for optimal cellular reactivity. The level of cellular sensitivity of approximately 200 ragweed-sensitive donors has been ascertained, and the kinetics of the release process studied. The rate of histamine release is a function of antigen concentration, but even with a large excess of this reagent it is impossible to abolish a lag phase. Chelation of the divalent cations or a decrease in the reaction temperature may be utilized to stop the reaction. These measures are effective both before and after the initiation of histamine release. Diminished cellular reactivity (desensitization) has been achieved by several procedures. These have in common the addition of antigen to cells in an environment deficient in but a single respect, followed by a restoration of optimal conditions. The significance of these data has been discussed and it has been proposed that immunologically induced histamine release is an active, enzymatically mediated process which occurs as a multistep response of viable cells to a specific antigenic stimulus.

Antigens↗
PubMed1967

Complement as a mediator of inflammation. II. Biological properties of anaphylatoxin prepared with purified components of human complement.

Interaction in free solution of highly purified preparations of human C'1 esterase, C'4, C'2, and C'3, in the presence of Mg(2+), resulted in rapid generation of an activity indistinguishable by biological criteria from anaphylatoxin. The formation of anaphylatoxin was associated with immunoelectrophoretic conversion of C'3 to anodically faster migrating proteins and was unaffected by the presence or absence of added C'5. The biological properties of human anaphylatoxin prepared in this manner include: contraction and desensitization of isolated guinea pig ileum, failure to contract isolated rat uterus, enhancement of vascular permeability in guinea pig skin, degranulation of mast cells in guinea pig mesentery preparations, and liberation of histamine from suspensions of rat peritoneal mast cells. The smooth muscle-contracting and permeability enhancing properties were fully blocked by an antihistaminic drug, triprolidine. No cross-desensitizing activity on guinea pig ileum was demonstrable between rat and human or guinea pig and human anaphylatoxins but a closer biological relationship between rat and guinea pig anaphylatoxins was observed. It is concluded that anaphylatoxin is a product of the complement system. Its possible relationship to apparently similar activities currently being obtained in other laboratories has been discussed.

Anaphylaxis↗
PubMed2001

Nitric oxide in primary headaches.

The molecular mechanisms that underlie the primary headaches-migraine, cluster headache and tension-type headache-have not yet been clarified. On the basis of studies in headache induced by intravenous infusions of glyceryl trinitrate (an exogenous nitric oxide donor) and histamine (which liberates nitric oxide from vascular endothelium), it has been suggested that nitric oxide is a likely candidate responsible molecule. The present review deals with the biology of this small messenger molecule, and the updated scientific evidence that suggests a key role for this molecule in primary headaches. This evidence suggests that the release of nitric oxide from blood vessels, perivascular nerve endings or from brain tissue is an important molecular trigger mechanism in spontaneous headache pain. Pilot trials have shown efficacy of a nitric oxide synthase inhibitor in both migraine attacks and chronic tension-type headache. These observations suggest new approaches to the pharmacological treatment of headache.

Enzyme Inhibitors↗
PubMed1980

Anaphylactoid reaction to infusion of polygelatin (Haemaccel). A study in pregnant women.

A series of allergic reactions to infusion of polygelatin (Haemaccel) in six pregnant women is reported. These women and a control group of five pregnant women were studied with analysis of complement, ELISA and skin tests. No differences were found between the groups in the factors studied. It is concluded that the reactions to polygelatin were caused through direct liberation of histamine, that is, an anaphylactoid reaction.

Anaphylaxis↗
PubMed1997

Anaphylactoid shock--a common cause of death in heroin addicts?

We measured mast-cell tryptase in postmortem blood from 22 heroin addicts dying suddenly after injection. In 32%, the concentration of tryptase was elevated (> or = 10 micrograms/l), and the mean value of tryptase was significantly different from a control group dying from known, nonimmunologic causes (P < 0.05). The increased tryptase concentrations indicate that death was preceded by systemic mast-cell degranulation. All victims of drug deaths had morphine in blood, most below 0.2 microgram/ml. In 71% of the victims of drug-related deaths with tryptase values > or = 10 micrograms/l, the intermediate degradation product, 6-monoacetyl-morphine, was not found in blood, whereas this was the case in only two victims with values below that cutoff point. This indicates that those with high tryptase concentrations survived longer than those with lower values. No correlation was found between the IgE levels and tryptase in either group, supporting the hypothesis that tryptase release was not mediated by an allergic reaction. The well-known property of opiates to stimulate unspecifically the liberation of histamine and other constituents of mast-cell granules offers one explanation of our observations. The results suggest that many heroin fatalities are caused by an anaphylactoid reaction.

Adult↗
PubMed1962

Inhibitory effects of carbohydrates on histamine release and mast cell disruption by dextran.

Alloxan diabetic rats failed to show the skin reaction (blue spot) evoked by dextran, whereas the effects produced by histamine and compound 48/80 were not altered. When dextran and glucose were injected simultaneously into the skin the reaction was inhibited. In vitro, mast cell alterations produced by dextran occurred simultaneously with histamine release; both processes were inhibited by glucose, other carbohydrates related to glucose, and inhibitors of anaphylaxis. These experiments suggest that dextran releases histamine by a mechanism similar to that found with 48/80 and anaphylaxis in the rat. The inhibitory effect of carbohydrates may be understood on the basis of a competitive mechanism.

Alloxan↗