[Inhibitory effect of nicardipine on 45Ca uptake and histamine release in rat mast cells stimulated by antigen].
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Biomedical subjects
Publications and source records attributed to H Kitani.
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The effect of PSK on the depressed bactericidal activity of macrophages and delayed-type hypersensitivity (DTH) to Listeria monocytogenes in BALB/c mice bearing transplantable Meth A fibrosarcoma was studied. In tumor-bearing mice pretreated with PSK, L. monocytogenes was cleared rapidly from the circulating blood and bacterial growth in the liver was inhibited effectively in the early phase of infection. This resistance to the infection could be transferred with adherent peritoneal exudate cells (PEC) but not with nonadherent or adherent spleen cells of PSK-treated mice. In the early phase of infection, tumor-bearing mice developed a lower level of DTH to L. monocytogenes than nongrafted control mice. However, the control levels of DTH could be obtained by pretreatment with PSK in tumor-bearing mice. These results suggest that the restoration of DTH to L. monocytogenes by pretreatment with PSK may be attributable to the restoration of the depressed immunological responsiveness to the normal levels in tumor-bearing mice.
The release of histamine by allergen and anti-IgE from whole blood was observed in 34 asthmatic subjects with a positive skin test to house dust. The time course of histamine release showed that the release by allergen and anti-IgE peaked after 15 min incubation. There was no significant difference in the time course of the release from whole blood between allergen and anti-IgE. Anti-IgE-induced histamine release correlated to a certain extent with the serum IgE level. Histamine release by house dust, on the other hand, correlated with the radioallergosorbent test score. A striking difference was present in the dose-response slope between allergen and anti-IgE. The maximum percent release correlated with the dose-response slope by allergen, but not by anti-IgE. The amount of histamine release induced by anti-IgE paralleled the amount of the release by house dust in the cases sensitive to the allergen; less sensitive basophils to anti-IgE were less sensitive to house dust.
The purification of the osteoblast-like cells (2-3%) among the bone marrow cells (BMC) of C57BL/6 mice using a specific anti-osteoblast serum and a fluorescence-activated cell sorter is described. The antiserum was raised against osteoblast cells isolated from calvaria from neonatal mice. The majority of the cells of the osteoblast-enriched fraction from bone marrow showed a parathormone-induced increase in cyclic adenine monophosphate but no response to calcitonin. This is similar to the response of osteoblast cells obtained from the calvaria. Electron microscopic studies of the extracellular matrix of cultured osteoblast-like cells purified from bone marrow showed the deposition of apatite crystals within and in close apposition to the vesicles. These findings suggest that the isolated cell population was enriched in osteoblasts. Such a cell system from bone marrow might provide an experimental system for investigating the mechanism of bone formation.
IgE-mediated histamine release from whole blood was analyzed in 44 patients with bronchial asthma by observing maximum present release and dose-response curves of histamine release induced by anti-IgE and house dust extract. The maximum histamine release from whole blood induced by anti-IgE correlated with total serum IgE levels. There was a close correlation between allergen-induced release from whole blood and the serum levels of specific IgE antibodies. In the maximum histamine release from whole blood induced by both anti-IgE and allergen, the interaction with a serum factor was not clearly recognized. Effect of a serum factor was shown in the dose-response curves of anti-IgE-induced histamine release, but not in those of allergen-induced histamine release. The dose-response curves caused by anti-IgE showed that basophils from cases with a high serum IgE level require much more anti-IgE to produce maximum histamine release than basophils from cases with a low serum IgE level. The results showed that IgE molecules contained in the serum participate in anti-IgE-induced histamine release from whole blood.
The correlation between blood eosinophilia and anti-IgE-mediated histamine release was investigated in 22 bronchial asthma patients with peripheral eosinophilia (over 8%). In the cases (Group A-1 and Group A-2) in which house dust was the specific antigen, significant histamine release from basophils was induced by anti-IgE and house dust. The result indicates a relationship between eosinophilia and the IgE-mediated mechanism of disease onset. In the cases (Group A-3) with RAST scores of 0+ and 1+ to house dust, the anti-IgE-induced histamine release varied from low to high percentages, and the participation of the IgE-mediated pathway was indicated in some cases. In the cases (Group B) with negative skin reactions, few patients had a family history of allergic disease. Their ages at onset were higher, and they demonstrated lower total IgE levels. These cases showed an extremely low percent of histamine release from basophils, which indicated the absence of a correlation between eosinophilia and IgE-mediated mechanisms.
Anti-IgE-induced histamine release from basophils was examined in 46 asthmatic subjects using a whole blood method. Basophils from subjects less than 30 years old released more histamine than those from subjects aged 41 to 50. The age at onset of the disease also affected the reactivity of basophils to anti-IgE: basophils showed a high response in subjects whose age at onset was between 0 and 10 years, and low response in the subjects whose age at onset was between 41 and 50 years. There was a correlation between histamine release and serum IgE levels. However, individual dose-response curves of histamine release varied greatly in whom serum IgE levels were low.
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The effect of PSK on the depressed interferon (IF) production in tumor-bearing mice was studied. In tumor-bearing mice, in vitro IF production by spleen cells treated with polyinosinic-polycytidylic acid (poly I:C) was remarkably inhibited. However, these inhibitions were prevented by the intraperitoneal (ip) administration of PSK. Mice were inoculated intravenously (iv) with poly I:C-treated spleen cells, administered with PSK ip at 3 days after the tumor inoculation. When PSK was not given, poly I:C-treated spleen cells did not show an inhibitory effect on tumor growth. In mice given PSK ip, poly I:C-treated spleen cells exerted slightly inhibiting effects on tumor growth. These results suggest that PSK prevented such a modulation in tumor-bearing mice.
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Effector mechanisms responsible for protection against ectromelia virus (EMV) including antiviral activity of non-immune macrophages, cytotoxic T cells, antiviral antibody, delayed footpad reaction to viral antigen and interferon induction after viral infection were depressed in BALB/c mice bearing syngeneic Meth A tumors. The degree of viral growth correlated well with the depression of delayed footpad reaction, antibody production and interferon induction. But a control level of these elements could be obtained by pretreatment of tumor-bearing mice, with PSK Cytotoxic activity may not be the principal effector, since cytotoxicity was induced in both normal and tumor-bearing mice to almost the same extent but an explosive viral growth was observed only in the latter. These results suggest that PSK was responsible for restoring the depressed antiviral protective immunity to normal levels in tumor-bearing animals.
Cellular accumulation to the peritoneal cavity and modification of various functions of peritoneal macrophages were observed in mice injected intraperitoneally (ip) with thioglycollate medium (TG), liquid paraffin, proteose peptone and Corynebacterium parvum. The cellular composition of peritoneal exudates at 4 days after injection of irritants was almost the same in all the groups and the proportion of macrophages was increased approximately 4 times more than nontreated controls. The ability to kill Listeria monocytogenes and to generate chemiluminescence (CL) were augmented strongly in C. parvum-induced macrophages, while depressed in TG-induced macrophages. The activities of liquid paraffin- or proteose peptone-induced macrophages were almost the same as those in nontreated controls. However, the ability to phagocytose native sheep erythrocytes was greatly augmented both in C. parvum- and TG-induced macrophages. There is thus a discrepancy between bactericidal activity and phagocytic activity among macrophages induced with various irritants.
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The metabolic pathway of 4-hydroxyaminoquinoline-1-oxide (4HAQO) and its binding to DNA was studied in 2-day chick embryos administered [G-3H]4HAQO in a shell-less culture. The 4HAQO rapidly metabolized into non-carcinogenic compounds and 1 h after administration only very small amounts of free 4HAQO could be detected in the embryo cells. The amount of DNA-bound 4HAQO in the embryo cells reached a maximum 2 h after administration, then began to decrease. The maximum extent (mu mol/mol P of nucleotide) was 18.2, equivalent to 1 molecule of 4HAQO-purine adducts per 2.8 X 10(4) base pairs of DNA. It was possible to detect removal of 4HAQO-purine adducts from DNA in chick embryo cells in a shell-less culture. A dose-response relationship for the killing effect of 4HAQO on 2-day embryos was observed in the range of 0.24-24 nmol 4HAQO per embryo. The practicality of the present method of administration of 4HAQO for 'flash administration' of compounds to chick embryo and the advantages of the shell-less culture method which provides access for biochemical and developmental studies of chick embryos were also discussed.
Effects of carrageenan and gamma-irradiation on virus titre in the liver were observed after intravenous inoculation of 8 X 10(3) p.f.u. of ectromelia virus which was not lethal for untreated mice. Trapping of virus by the liver within 30 min and an initial transient reduction in titre by day 1 were not affected by gamma-irradiation but were inhibited by pretreatment with carrageenan. An increase from day 1 to day 3 was not affected by gamma-irradiation but was augmented by pretreatment with carrageenan. Therefore, protection within 3 days may depend principally upon carrageenan-sensitive and irradiation-resistant cells, namely, fixed macrophages. Elimination of virus from day 4 to day 7 depended upon cell-mediated immunity. When carrageenan was given 3 days after virus inoculation, the titre of virus increased progressively from day 4 ultimately to kill the hosts. The cytotoxic activity of spleen cells against infected target cells was raised in carrageenan-treated mice as well as in untreated mice. Immune elimination of virus may be mediated by a mechanism requiring the cooperation of sensitized T lymphocytes and blood monocytes.