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Biomedical subjects

M Kaliner

Publications and source records attributed to M Kaliner.

At least 127 records · Page 7Linked to original sources
PubMed1979

Human platelet arylsulphatases: identification and capacity to destroy SRS-A.

Arylsulphatases IIA and IIB have been separately identified in human platelets by use of anion exchange chromatography and gel filtration. Arylsulphatase IIA had a molecular weight of 160,000 and a pH optimum of 4.5. Arylsulphatase IIB had a molecular weight of 60,000 and a pH optimum of 5.5. Both arylsulphatases IIA and IIB were inhibited by phosphate and sulphate ions characteristic of this enzyme class. Platelets, upon exposure to ionophore A-23187 or thrombin, discharged arylsulphatase coincident with beta-glcuronidase release. Partially purified platelet arylsulphatase IIB inactivated rat SRS-A.

Arylsulfatases↗
PubMed1978

Human lung tissue and anaphylaxis: the effects of histamine on the immunologic release of mediators.

The IgE-mediated, antigen-induced release of histamine from human lung tissue causes profound changes in lung cyclic adenosine monophosphate and cyclic guanosine monophosphate. Exogenous histamine similarly induces increases in both cyclic nucleotides; pretreatment with H-1 antihistamines prevents the increase in cyclic guanosine monophosphate, whereas H-2 antihistamines prevent the increase in cyclic adenosine monophosphate. Anaphylaxis of human lung in vitro is unaffected by the presence of 1-100 micron histamine, H-1 antihistamines, H-2 antihistamines, or combinations of these agents despite the production of selective increases in total lung cyclic nucleotides. Futhermore, selective histamine agonists (2-methylhistamine [H-1 agonist] or dimaprit [H-2 agonist]) also fail to significantly influence the immunologic release of mediators. Histamine examined in the presence of ethylenediaminetetra-acetate was no more capable of modulating mediator release than when in the presence of calcium, in contrast to previous studies involving the human basophilic leukocyte. Therefore, the human lung mast cell is unresponsive to histamine with regard to modulating the antigen-induced, IgE-dependent, generation of mediators.

Antigens↗
PubMed1978

Immunologic and nonimmunologic generation of superoxide from mast cells and basophils.

Mediator release from rat peritoneal and human lung mast cells as well as human leukemic basophils was examined to determine whether super-oxide (O(-) (2)) was concomitantly generated. Immunologic or nonimmunologic stimulation of each preparation induced parallel release of histamine and O(-) (2) within 2 min. O(-) (2) production was quantitated by superoxide dismutase (SOD)-inhibitable chemiluminescence and cytochrome c reduction. SOD was detected in basophil and mast cell lysates and was also released by rat mast cells stimulated by anti-IgE. Secretory granules isolated from purified rat mast cells released histamine, O(-) (2), and SOD upon exposure to cations. Thus, both superoxide radicals and SOD may play a role in host defenses involved in immediate hypersensitivity reactions.

Animals↗
PubMed1978

The effects of the immunologic release of histamine upon human lung cyclic nucleotide levels and prostaglandin generation.

The effect of the antigen-induced, immunoglobulin (Ig)E-dependent release of mediators from human lung tissue was analyzed for coincident changes in the tissue levels of cyclic nucleotides. Simultaneously with the appearance of mediators, lung cyclic guanosine 3',5'-monophosphate (GMP) increased from 0.9+/-0.2 to 12.63+/-4.5 pmol/mg protein and cyclic AMP increased threefold from the initial levels of 5.1+/-1.4 pmol/mg protein. The release of histamine and prostaglandin (PG)F(2alpha), as well as the associated increases in cyclic nucleotides, peaked within 10 min of anaphylaxis. Antagonists of histamine's H-1 receptor prevented anaphylaxis-associated increases in cyclic GMP, whereas H-2 antagonists prevented the cyclic AMP response. Neither of these antagonists influenced the pattern or quantity of histamine or slow-reacting substance of anaphylaxis release. Prevention of PGF(2alpha) synthesis with acetylsalicylic acid failed to influence histamine or slow-reacting substance of anaphylaxis release or the concomitant increases in cyclic nucleotides. Histamine, added exogenously, produced a prompt increase in the cyclic AMP and cyclic GMP levels of human lung. As was seen after anaphylaxis, H-1 anatagonists prevented the cyclic GMP response to histamine, whereas H-2 antagonists prevented the cyclic AMP response.H-1 antagonists prevented 50% of the PGF(2alpha) synthesis accompanying anaphylaxis; H-2 antagonists had no effect. Exogenous histamine induced PGF(2alpha) synthesis; this synthesis was prevented by H-1 but not H-2 antagonists, and was reproduced by 2-methylhistamine (H-1 agonist) but not by dimaprit (H-2 agonist). Arachidonic acid generation of PGF(2alpha) was not influenced by antihistamines. Therefore, histamine interactions with human lung result in the synthesis of both PGF(2alpha) and cyclic GMP in response to H-1 stimulation, and of cyclic AMP through H-2 stimulation.

Anaphylaxis↗
PubMed1977

Human lung tissue and anaphylaxis. I. The role of cyclic GMP as a modulator of the immunologically induced secretory process.

A close relationship between increased concentrations of cyclic GMP in human lung tissue and the capacity for acetylcholine to enhance the immunologic secretion of histamine and SRS-A has been found. Acetylcholine (10(-7) to 10(-11) M) produced parallel increases in both cyclic GMP and the immunologic release of mediators; the muscarinic blocking agent atropine prevented both responses. The increase in cyclic GMP in human lung after acetylcholine stimulation was apparent within 30 sec, peaked by 120 sec, and abruptly returned to control levels thereafter. The ability of acetylcholine to enhance the antigen-stimulated secretion of mediators followed the same time-course. PGF2alpha (3.3 X 10(-4) M to 3.3 X 10(-7) M) increased the cyclic GMP content of human lung tissue in a dose-related fashion. Pretreatment of IgE-sensitized lung tissue with acetylsalicylic acid (10 microgram/ml) had no effect on baseline cyclic nucleotide levels, the capacity for antigen to induce mediator release, or the increase in cyclic GMP and facilitation of the immunologic release of mediators produced by acetylcholine.

Acetylcholine↗
PubMed1977

Human lung tissue and anaphylaxis. Evidence that cyclic nucleotides modulate the immunologic release of mediators through effects on microtubular assembly.

The addition of specific antigen to IgE-sensitized human lung tissue causes the secretion of the mediators histamine and slow-reacting substance of anaphylaxis. The mechanisms by which increased levels of cyclic AMP suppress and increased levels of cyclic GMP enhance this secretory process were studied. Colchicine, an agent which disrupts many secretory reactions by binding to microtubules in their disassembled 6S form, was a relatively ineffective inhibitor of the antigen-induced release of mediators unless lung fragments were incubated at 4 degrees C for 60 min to induce microtubular disassembly. As colchicine appeared to inhibit the immunologic secretion of mediators from human lung tissue most effectively after microtubular disassembly, the capacity of colchicine to modulate the release reaction indicated the state of microtubular assembly; inhibition by colchicine signaled a shift to the colchicine-sensitive 6S subunits whereas failure to inhibit suggested maintenance in the colchicine-resistant polymerized state.Exogenously added 8-Bromo-cyclic GMP prevented low temperature-facilitated colchicine suppression of mediator release suggesting that increased levels of cyclic GMP stabilize polymerized microtubules. Transiently increased cyclic AMP concentrations, either exogenously added as 8-Bromo-cyclic AMP or endogenously produced by isoproterenol, promoted colchicine suppression of mediator release suggesting that microtubular disassembly was produced. Direct measurement of cyclic AMP levels revealed parallel kinetics after isoproterenol stimulation between control and colchicine-treated lung fragments. The requirement for functional microtubules in the release reaction may occur after the antigen IgE-stimulated activation of a serine esterase, energy utilization, and an intracellular calcium requirement. The mechanism by which cyclic nucleotides influence microtubular assembly is postulated to involve the degree of phosphorylation-dephosphorylation of microtubules.

Anaphylaxis↗
PubMed1976

The cholinergic nervous system and immediate hypersensitivity. 1. Eccrine sweat responses in allergic patients.

The cholinergically innervated human eccrine sweat gland is a readily available organ permitting the assessment in allergic patients of cholinergic reactivity with few or no adrenergic influences. The sweat responses of four matched groups (male allergic, female allergic, male control, and female control) to intradermal Mecholyl from 0.1 mug to 100 mug was compared; the 45 male and 45 female allergic patients demonstrated statistically significant increases in sweat responses to essentially all concentrations of Mecholyl examined. No difference in the sweat responses of patients with allergic rhinitis alone was compared with patients with both allergic rhinitis and allergic asthma was noted. Five patients with intrinsic asthma most closely resembled the allergic groups in their responses and 8 patients with vasomotor rhinitis sweated at or below the control groups. The increased sensitivity of allergic patients to cholinergic stimulation as measured by eccrine sweat responses suggest that this hyperresponsiveness may be one of the underlying defects in allergic disease.

Contraceptives, Oral↗
PubMed1974

Symposium on allergic lung disease. IV. Immunologic mechanisms for release of chemical mediators of anaphylaxis from human lung tissue.

The antigen-induced, IgE-dependent release of chemical mediators from human lung tissue in vitro is modulated by a variety of pharmacologic maneuvers involving alterations in the intracellular levels of cyclic nucleotides. Increase in the level of cyclic AMP inhibits the immunologic release of histamine, SRS-A and ECF-A; beta-adrenergic agents, prostaglandins, cholera toxin and methylxanthines all produce accumulations of cAMP in human lung tissue. Depletion of cAMP after alpha-adrenergic, low-dose prostaglandin and imidazole stimulation is associated with enhancement of the release of mediators. Studies involving purified preparations of rat peritoneal mast cells confirm that alterations in the cAMP levels of a homogeneous population of target cells indeed influence histamine release in a fashion analogous to that of human lung tissue.Furthermore, cholinergic stimuli produce a marked enhancement of the antigen-induced release of mediators from human lung through an apparently independent mechanism, presumably acting through alterations in the tissue concentration of cyclic GMP. This latter observation suggests an important interaction between endogenously released parasympathetic neurohormones and the immunologic release of the chemical mediators of asthma.

Anaphylaxis↗
PubMed1974

Adenosine 3'5'-monophosphate: inhibition of complement-mediated cell lysis.

An increase in adenosine 3',5'-monophosphate (cyclic AMP) in rat mast cells, achieved by stimulating the cells with prostaglandin E(1), by preventing cyclic AMP breakdown with aminophylline, or by adding exogenous dibutyryl cyclic AMP, prevented complement-mediated cytolysis as assessed by both histamine release and vital dye exclusion. Dibutyryl cyclic AMP also suppressed water-induced osmotic lysis.

Aminophylline↗