Biomedical subjects
Publications and source records attributed to M Ohta.
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Interferon production stimulated by the active substance (neutral fraction) of the capsular polysaccharide of Klebsiella pneumoniae (neutral CPS-K) in BCG-infected mice was compared with that by bacterial lipopolysaccharide (LPS). Prior infection with BCG increased the responsiveness of mice to the lethal effect of neutral CPS-K as well as to that of LPS. Associated with this, BCG-infected mice showed a markedly enhanced ability to produce interferon after stimulation not only by LPS but also by neutral CPS-K. In addition, a cytotoxic factor (cytotoxin) was found to be released in the serum of BCG-infected mice after injection of these inducers. The kinetics of production of interferon and cytotoxin stimulated by neutral CPS-K were very similar to those stimulated by LPS. The time pattern of cytotoxin production was not in parallel with that of interferon production. Interferon reached a peak 2 hr and cytotoxin 3 hr after injection with these inducers. Interferon and cytotoxin produced by neutral CPS-K showed essentially the same stabilities to heating at 56 C and to treatment at pH 2 respectively as those produced by LPS. Interferon was inactivated by heating at 56 C more rapidly than cytotoxin. Cytotoxin was inactivated by treatment at pH 2 for 24 hr, whereas interferon activity was well preserved after this treatment. These results suggest that both activities are the result of different substances.
The time course of the occurrence of hyperreactivity in interferon and cytotoxin responses to the active substance (neutral fraction) of the capsular polysaccharide of Klebsiella pneumoniae (neutral CPS-K) and bacterial lipopolysaccharide (LPS) and of the hyperreactivity to their lethal effects was followed after infection with BCG in SMA and ICR strains of mice. The duration of these hyperreactivities of BCG-infected mice depended on the inoculum doses of BCG. The time patterns of the hyperreactivity to the lethal effects of neutral CPS-K and LPS were similar in both strains of mice, although the maximum toxicity of LPS by the intraperitoneal route in BCG-infected mice on a weight basis was stronger than that of neutral CPS-K. Irrespective of inducer and mouse strain, the time pattern of the hyperreactivity to produce cytotoxin was similar to that of the hyperreactivity to produce interferon. The patterns for these phenomena when neutral CPS-K was used as an inducer were also similar to those when LPS was used. In ICR mice the hyperreactivity in interferon and cytotoxin responses to either neutral CPS-K or LPS decayed significantly earlier than the hyperreactivity to their lethal effects, whereas in SMA mice the occurrence of both types of hyperreactivities seemed to be associated. Therefore, it is suggested that the mechanism for the hyperreactivity in interferon and cytotoxin responses to neutral CPS-K or LPS in BCG-infected mice is not necessarily the same as that for the hyperreactivity to their lethal effects.
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This paper is concerned with the adjuvant activity in stimulatory immunoglobulin E production against ovalbumin (OA) by bacterial cell walls, cell wall peptidoglycan (PG), and their PG fragments and synthetic N-acetylmuramyl (MurNAc) dipeptides in A/J mice. A PG isolated from Streptococcus pyogenes, PG subunit polymer and dimer obtained from Staphylococcus epidermidis, and water-soluble fragments of cell walls or PG prepared from Nocardia corynebacteriodes and Streptomyces gardneri were found to enhance both the primary and secondary responses of anti-OA immunoglobulin E antibody production. It was suggested that the PG portion, either intact or highly degraded, was capable of enhancing the immunoglobulin E antibody production, and there was no need for the non-PG moiety or intactness of PG structure for the adjuvant activity. This finding was confirmed and extended by the use of synthetic MurNAc dipeptides. Among eight MurNAc dipeptides tested, MurNAc-l-Ala-d-isoGln, MurNAc-l-Ala-d-Gln, MurNAc-l-Ala-d-Glu, and MurNAc-l-Ser-d-isoGln were found active as an adjuvant in the stimulation of the primary and secondary reaginic anti-OA antibody production in a similar way to the cell wall PG and their fragments. None of the synthetic MurNAc-l-Ala-l-isoGln, MurNAc-l-Ala-l-Gln, MurNAc-l-Ala-l-Glu, and MurNAc-l-Ala-d-isoAsn, on the other hand, stimulated the anti-OA immunoglobulin E antibody production in either primary or secondary response, indicating the importance for the adjuvancy in immunoglobulin E production of the configuration of the glutamic acid residues adjacent to the l-Ala (or l-Ser) in muramyl dipeptides.
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Nonspecific adjuvant immunotherapy with Bacillus Calmette-Guérin cell wall skeleton (BCG-CWS) was given to 155 lung cancer patients. Clinical effects of the BCG-CWS treatment were estimated by comparing the survival of the BCG-CWS group with that of a historical control group on the basis of 4-year results. Significant prolongation of survival time has been observed in Clinical Stages II, III (M0) and III (M1). However, most Stage III patients who were given the BCG-CWS treatment died of cancer itself after marked prolongation of survival time. An increase in complete cure rate has been expected only in Stages I and II. Surgicopathological staging was used in resected cases. Resected cases at any stage were sensitive to treatment with BCG-CWS. Histologically, all types of lung cancer including squamous cell carcinoma, adenocarcinoma, and anaplastic carcinoma were sensitive to treatment with BCG-CWS. Intrapleural administration of BCG-CWS to patients with malignant pleurisy was effective in controlling the pleural effusion and prolonging the survival time. No serious complication has been experienced in our study.
Cytostatic acitivity of peripheral blood monocytes against cultured cell lines of bronchogenic carcinoma was examined in patients with lung cancer. Cytostatic activity in lung cancer patients with neither augmented nor suppressed as compared with that of controls such as normal healthy persons, patients with malignancies other than lung cancer, and patients with benign respiratory diseases. There was no correlation between the cytostatic activity of monocytes and the advance of clinical stages of the disease. Conventional modalities of anticancer treatments such as surgery, radiotherapy, chemotherapy, and their combination therapy had no effect on cytostatic activity of peripheral blood monocytes. However, adequate immunotherapy with nocardia rubra cell-wall skeleton augmented the cytostatic activity of peripheral blood monocytes, although adequate immunotherapy with Mycobacterium bovis BCG cell-wall skeleton had no effect.
The ageing processes in dental Ag-Pd-Cu-Au alloy were investigated by means of electrical resistivity measurements during anisothermal annealing. The main results obtained are as follows; (1) There are two obvious precipitation processes (stage I and stage II) during anisothermal annealing after quenching from above critical temperature. And the apparent difference in stage I attribute to solution treatment temperature. (2) Stage I occured at lower temperature, is one ageing process by the migration and annihilation of quenched-in excess vacancies. Another is stage II at higher temperature by the diffusion of equilibrium vacancies.
Antitumor activity induced by the oil-attached cell-wall skeleton of Nocardia rubra (N-CWS) was compared with that of the oil-attached cell-wall skeleton of Mycobacterium bovis BCG (BCG-CWS) in syngeneic BALB/c tumor-host systems. In normal BALB/c mice (+/+), N-CWS exhibited stronger suppressive effect on syngeneic Br-1 and MCA tumors than did BCG-CWS. In athymic nude mice (nu/nu), BCG-CWS was as effective as N-CWS for the suppression of growth of such tumors. Suppressive effect of N-CWS treatment appears to be stronger to some extent in +/+ mice than in nu/nu mice. Immune spleen cells obtained from +/+ mice after footpad inoculation of MCA tumor cells mixed with N-CWS were effective in suppressing the MCA tumor growth, although those obtained from mice after inoculation of MCA tumor cells mixed with BCG-CWS did not exhibit a suppressive effect. This antitumor activity of immune spleen cells may be attributed to tumor-specific killer T cells. The differences of antitumor activities induced by these agents were discussed with reference to T-cell dependency and independency.
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Cytotoxicity of peripheral blood lymphocytes against allogeneic target cells of bronchogenic carcinoma was examined by a microcytotoxicity test before, during, and after radiotherapy in primary lung cancer patients. Before the treatment, cytotoxicity was depressed only slightly in patients in stage III and strikingly in those in stage IV, as compared to the values in patients at earlier stages of lung cancer such as stages I AND II. Local irradiation scarcely affected cytotoxicity at stages II and III, but augmented remarkably at stage IV. The number of peripheral blood lymphocytes decreased profoundly during and after radiotherapy in all cases of stages II, III, and IV. Although radiotherapy exhibited various effects on the cytotoxic activity of lymphocytes and the number of peripheral blood lymphocytes, only the cytotoxic activity at the end of radiotherapy correlated well with the reduction in tumor size.
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