[Ultrastructural study of the basophilic granural cells in allergic nasal secretion and mucous membrane (author's transl)].
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Biomedical subjects
Publications and source records attributed to M Okuda.
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Evidences on the important role of tissue mast cells in inducing allergy have accumulated. There cells are known to be present in nasal secretion but have not been well studied. In the present study basophilic cells containing granules which stained metachromatically appeared in the nasal secretion in various kinds of inhalant allergy. An increase in their number was observed after nasal provocation and during the pollinosis season and showed a decrease after a course of immunotherapy or during the off-season of pollinosis. They were well correlated in degree with nasal symptoms, nasal eosinophilia, and nasal provocative reactions. These results suggest that the appearance of the basophilic cell in nasal secretion is related to their specifity in nasal allergy. The possibility of onset of nasal allergy due to the release of chemical mediators from basophilic cells in nasal secretion was discussed.
The methodology of the provocative nasal test has varied according to the investigators. In order to establish a standard method of this test quantification of the nasal challenge, including the amount of the allergen, nasal site, side and size of allergen deposition, was studied. From the results obtained it is preferable to use the end point test and to apply allergen to the anterior part of the inferior turbinate in a 7mm2 size of surface area, bilaterally. An alternative test is to use a fixed amount of allergen (500 mug house dust in house dust allergy).
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Nerve cell bodies, large and multipolar, were isolated in bulk with the least possible contamination from the pig brain stem. The activities of two neurobiologically important membrane enzymes, Na+, K+-ATPase, and acetylcholinesterase, in the isolated cell bodies were estimated. Na+, K+-ATPase [EC 3.6.1.4], more accurately called ouabain-sensitive ATPase of the nerve cell body, hydrolyzed 94 micronmoles of ATP per h per 100 mg of protein. This activity was one-fourth that in the brain stem. Nerve cell bodies contained a large amount of Ca2+, 275 micronmoles per 100 mg of protein, about half of which was calculated to exist as compounds other than calcium orthophosphate. However, the Na+, K+-ATPase of the nerve cell bodies was not stimulated by EGTA, in contrast to that of the brain stem. Acetylcholinesterase [EC 3.1.1.7] and cholinesterase [EC 3.1.1.8] activities were estimated separately by the use of the specific inhibitors Persidol and BW 284C51 dibromide. Acetylcholinesterase was almost completely responsible for the hydrolysis of acetylcholine in the nerve cell bodies isolated from the brain stem and little cholinesterase activity was detected. 1300-1400 micronmoles of acetylcholine was hydrolyzed per h per 100 mg of protein of the neuronal cell bodies; this activity was about four times higher than that in the brain stem. The differences between the specific activities of Na+, K+-ATPase, and acetylcholinesterase in theneuronal cell bodies and the brain stem are discussed in the light of electron microscopic analysis of the distribution of these enzymes and the preservation of the plasma membrane of the isolated cell bodies.
Much peroxidase is released from eosinophils that ingest complexes formed of human immunoglobulins with specific rabbit antibody. The complex formed of IgE with rabbit antibody, was particularly effective. The amount and rate of release of peroxidase was closely related to the amounts of complex ingested by the eosinophils, and degree of lysis of the cell granules. It is proposed that eosinophils attracted to an allergic lesion ingest complexes of IgE, show lysis of granules with release of peroxidase, and that the peroxidase reduces the allergic reaction.
The tissue uptake of 3H-methylprednisolone (3H-MP) was studied in anesthetized cats during acute myocardial ischemia 1 and 2 hours after injection of 3H-MP. There was a rapid uptake of 3H-MP by many tissues. Liver, kidney, and pancreas exhibited tissue/perfusion ratios of 3 to 7, heart, lungs, and intestine about 2, spleen, adrenal, and aorta 1 to 2, and skeletal muscle and omentum less than 1. Very similar tissue uptakes occurred in cats subjected to myocardial ischemia and sham myocardial ischemia at 1 and 2 hours. Plasma clearances of 3H-MP was not significantly altered either 1 or 2 hours after the onset of myocardial ischemia. Although ischemic myocardial tissue took up less than nonischemic myocardial tissue, this region accumulated significant amounts of 3H-MP. Myocardial tissue metabolized only about 15 to 20 per cent of the 3H-MP taken up after 2 hours. These data indicate that in acute myocardial ischemia, myocardial tissue takes up large amounts of exogenously administered glucocorticoid, most of which remains in the native form during the early phase of acute myocardial infarction.
Immunoglobulins of different classes are known to play a role in humoral defense mechanism, and Immunoglobulin E, without any actual evidence, is also expected to perform the same function. From the point of the defensive role the present study was undertaken in nasal allergy by observing the way in which powdered carbon particles previously insufflated in the nasal cavities are rapidly removed by nasal provocation with a causative allergen extract. The ratio of disapperance time of the carbon powder after/before provocation decreased markedly in good proportion with the intensity of the provocative reaction. Both sneezing and nasal secretion provocated contributed to this removal of the powder. When the nasal cavity on one side only was provocated, the non-provoked side also showed a rapid disappearance of the powder. In conclusion, Immunoglobulin E serves as a gate keeper by removing allergens from the surface of the nasal mucous membrane and by inhibiting the penetration of allergens into the nasal mucous membrane.
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Increase of serum IgE with frequent localization of IgE in the germinal centres, mast cell hyperplasia in lymph nodes and changes of specific granules in the infiltrated eosinophils, such as roughness of the matrix and appearance of tubular structures together with fusing and disappearance of the core, were demonstrated in eosinophilic granuloma of the soft tissue, so-called Kimura's disease, in association with increase of anti-Candida IgE antibody. It is suggested that this disease may be due to atopic allergy to Candida albicans.
We studied the uptake of labeled dexamethasone (3H-Dex) or methylprednisolone (3H-MP) in isolated perfused cat hearts during the first hour of acute myocardial ischemia. Considerable amounts of 3H-Dex and 3H-MP were taken up by the plasma membrane (F1) fraction in control, border zone, and ischemic myocardial tissue. Lesser amounts were incorporated into the remaining cell fractions. A gradient of glucocorticoid uptake was observed that decreased from control tissue to ischemic tissue in all subcellular fractions (i.e., F1 to F5). Accordingly, supernatant fraction (S) to particulate (P) ratios of labeled glucocorticoid uptake increased from control to ischemic tissue, indicating that myocardial cell damage resulted in a decrease in glucocorticoid-binding capacity in subcellular fractions obtained from ischemic tissue. The activity of 5'-nucleotidase (5'ND), a plasma membrane marker in myocardial cells, also decreased from normal to ischemic tissue. Furthermore, we found that uptake of 3H-MP and 3H-Dex was associated with the retention of 5'ND activity in F1 fractions of both border zone and ischemic tissue. Similar protection of plasma membrane integritg occurred in the supernatant fraction as determined by changes in S/P ratios of 5'ND activity. These data provide support for the concepts that (1) plasma membrane changes occur soon after acute myocardial ischemia, and (2) the mechanism by which glucocorticoids exert a protective effect in myocardial ischemia may be related to membrane stabilization.