[Cholinergic variant of noninfectious allergic bronchial asthma].
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Biomedical subjects
Publications and source records attributed to A D Ado.
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The paper deals with the investigation of endorphin content in the blood of patients with asthma. The increase in alpha- and beta-endorphin concentration was shown to depend on the severity of clinical manifestations of infectious-allergic and atopic forms of bronchial asthma. This regularity was not observed for gamma-endorphin. The infectious-allergic form of asthma was characterized by drastic reduction in the content of all three endorphin types upon treatment with dexamethasone. The possible role of endorphin reactions in the pathogenesis of asthma is discussed.
A study was made of the effects of the neurotransmitters acetylcholine and adrenaline on proliferation of B lymphocytes of mice immunized with ovalbumin. The neurotransmitters were noticed to be capable of changing B cell proliferation on cultivation in vitro. The effect (an increase or reduction of 3H-thymidine incorporation) depended on the time of immunization, antigen dose, and the type of a neurotransmitter. On the whole the pattern of the acetylcholine effect correlated with a natural trend of changes in B lymphocyte proliferation at different times of the immune response. Adrenaline produced a reciprocal effect.
Spontaneous velocity sedimentation of B lymphocytes activated by intraperitoneal injection of ovalbumin into mice was used to obtain cell cycle synchronized cells, evidenced by differences in the incorporation of labeled precursors of protein and nucleic synthesis (14C-methionine and 3H-thymidine). The effects of acetylcholine and adrenaline, cAMP and cGMP on the intensity of 3H-thymidine incorporation into mouse B lymphocytes and on the amount of the cells entering mitosis were examined. It was shown that acetylcholine is capable of stimulating whereas adrenaline of inhibitin B lymphocyte entry into the stage of DNA synthesis and egress of these cells from the stage of DNA synthesis to the stage of mitosis. Adrenaline was found to have a reciprocal action. The acetylcholine effect could be mimetized by exogenous cGMP, that of adrenaline by cAMP. Stimulation of the G1/S transition was mediated by intracellular calcium ions but did not depend on exocellular calcium.
A study was made of the action of a specific muscarinic antagonist 3H-quinuclidinyl benzylate on the immune rosette formation in BALB/c mice. It was shown that treatment of mouse spleen lymphocytes by 3H-QNB at a concentration of 10(-9) M-10(-14) M brought about rosette formation inhibition. The process was dose-dependent. Atropine reversed the action of 3H-QNB.
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Study of the effects of acetylcholine, exogenous cGMP and Con A on the mobility of B lymphocytes has demonstrated that an increase in both the content of cGMP and calcium in B lymphocytes stimulates their mobility. The measurement of intracellular content of cGMP in B lymphocytes by radioimmunoassay has shown that this content changes rapidly in response to the action of acetylcholine and that it is dependent but negligibly on extracellular calcium. The dependence of the effects of all three substances on trifluoperazine, a calmodulin v blocker, indicates that stimulation of B lymphocyte mobility is ultimately determined by the calcium mechanisms.
It was shown that B lymphocyte motility activated by anti-immunoglobulin serum may be abrogated in a Na+-deficient medium and in a 10(-5)M trifluoperazine-containing medium but not in a Ca2+-deficient medium. The tetracycline fluorescence test demonstrated Ca2+ efflux from isolated B lymphocyte mitochondria due to Na+ exposure. The radioimmunoassay demonstrated the cGMP level to rise after exposure to anti-immunoglobulin serum. The Na+-dependent Ca2+ efflux from the mitochondria might be the main mechanism in anti-immunoglobulin serum activation of B lymphocytes and in the cGMP level rising.
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The effect of neisserial sensitization on the protein spectra and phospholipid composition of acetyscholine receptor-rich membrane fragments was investigated in rat skeletal muscles. The sensitization led to substantial changes in the protein spectrum of the cell membranes of the skeletal muscles with high receptor activity in respect to choline. The phospholipid composition of the membranes was found to experience profound transformations. A considerable increase was noted in the content of sphingomye lin and phosphatidylcholine together with a marked drop in the content of phosphatidylethanolamine, phosphatidylinosite and phosphatidylserine.
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During sensitization of BALB/c mice to protein antigen, spontaneous and acetylcholine-induced mobility of spleen lymphocytes increased, the maximum being reached on days 1-3 from the sensitization commencement. The acetylcholine-induced mobility of lymphocytes was reduced if the lymphocytes had been preexposed to the antigen. The data obtained attest to the same cellular substrate of antigen and acetylcholine effects.
The effects of some choline compounds (acetylcholine, benzoylcholine, phosphorylcholine) on immune rosette-formation were studied in experiments on 150 BALB/c mice immunized with sheep red blood cells. Low concentration of the choline-containing substances (from 10(-14) to 10(-12) M) stimulated immune rosette-formation, whereas high concentrations (from 10(-8) to 10(-5) M) inhibited it. The blockade of lymphocyte cholinoreceptors with atropine reversed the action of phosphorylcholine on the processes of rosette-formation. Interaction of immune and mediator receptors is discussed.