The Kitasato archives of experimental medicine最新文献

The quality of 14 lots of acellular pertussis-diphtheria-tetanus (AC-PDT) vaccines manufactured by the Kitasato Institute during the period 1987-1990 were investigated. The geometric means of HSU, LPU, and BWDU were 0.078, 0.257, and 7.33 per ml respectively. The potency was higher than 14 IU per ml. These results indicated the consistency of the Kitasato AC-PDT vaccines. The antibody response to the AC-PDT vaccines was measured in primary and secondary vaccinated mice by ELISA. IgG antibody response to FHA and PT was obtained in all immunized mice (P less than 0.001) after the primary injection. In contrast, IgG antibody response to fimbriae 2 showed a significant titer rise (P less than 0.001) after the booster injection. The results indicated that the Kitasato AC-P vaccines consisted of protein, PT and FHA as the major antigens, and a little agglutinogen as the minor antigen.

Microelectrode and stereotaxic technique were used to record extracellular potentials of the neuron in posterior group of thalamic nuclei (PO). To study the action of some neural structures in the brain, we also applied the method of conditioning-testing stimulation. We found not only somatic nociceptive but visceronociceptive neurons existed in PO. The features of the unit response (latency, discharges and its noxious properties) were studied. Stimulation of S1, cingulate gyrus, caudate nucleus, accumbens, amygdala, habenula, VPL, PAG and substantia nigra caused inhibition of nociceptive neurons in PO. Owing to emerge and recover, the inhibition can be divided into three phases: prompt, continued and delayed. All these inhibitions except VPL, Cad and SN (no observation), were reversed by Naloxone. Both stimulation of somatic peripheral nerve fibers and electroacupuncture of Sanli (S36) on the hind leg of the cat produce suppression of nociceptive neuron in PO. The mechanism of inhibition resulted from above neural structures of the brain was also discussed.

To clarify the influence of lead on the host's defense mechanisms, antibody production in mice pretreated with lead was tested using the hemagglutination titer against SRBC (Sheep Red Blood Cells) and HRBC (Hamster Red Blood Cells) as indicator and the following results were obtained. 1. When mice were pretreated intraperitoneally with lead one day or six days before immunization and then immunized with SRBC, which is known as a strong antigen, antibody developed smoothly in the first immunization showing the same tendency as that of the control group. After the booster immunization, antibody production was markedly suppressed in the group of mice pretreated with lead six days before the immunization. When mice were immunized with HRBC, which is known as a weak antigen, antibody production was very poor in the first immunization, but after the booster immunization, the antibody titers rose rapidly in the group pretreated one day before the immunization. However, the titers of the group pretreated with lead 6 days before the immunization was considerably suppressed, showing the same tendency as that of mice immunized with SRBC. 2. When mice received intraperitoneally three or six doses of lead before immunization with SRBC or HRBC, antibody titer of these groups were somewhat lower than that of the control group. 3. When mice were pretreated intravenously with lead one day or six days before immunization with SRBC or HRBC, the antibody production ability was not remarkably damaged, showing almost the same titer as in the control group.

The antigen-dependent proliferative response of the Ia- T lymphocyte population in peritoneal exudate cells (PEC) of C3H/HeN mice immunized with horse red blood cells (HRBC) was examined by determining the uptake of tritiated thymidine ([3H]TdR) into the cells in vitro. Both the antigen and accessory cell population, which was either macrophages or B lymphocytes that had been prepared from the PEC or spleen of unimmunized mice, were necessary for the proliferative response of the Ia- T cell population and also the production of IL-2 by the Ia- T cells, but the Ia- T cell population could proliferate in the absence of antigen and accessory cells, if IL-2 was present. The IL-2-dependent proliferation of the Ia- T cells was augmented in the presence of macrophages, but not B cells. The Ia- T cells that had been treated previously with anti-IL-2 receptor (IL-2R) antibody showed no response to IL-2 in the presence or absence of B cells, but responded to IL-2 in the presence of macrophages. Direct contact of the Ia- T cells with macrophages seemed to be necessary for augmentation of the proliferative response of the Ia- T cells to IL-2 because the separation of these cell populations by a membrane filter in a Marbrook type culture vessel resulted in poor augmentation of the response. Cell-associated IL-1 did not participate in the augmentation because paraformaldehyde-treated macrophages did not help the response. When the Ia- T cells had been previously treated with complement and anti-asialo GM1 antibody, the IL-2-dependent proliferative response was not affected, but the augmentation of the response by macrophages was blocked. Previous treatment of the cells with anti-L3T4 antibody diminished the response to IL-2, but did not affect the augmentation of the response by macrophages. Pretreatment of the cells with anti-Thy-1.2-antibody reduced the response to IL-2 and the augmentation by macrophages. Therefore, we concluded that there are at least two populations, capable of responding to IL-2 in the immune Ia- T cell population; one with L3T4 surface antigen and another with asialo GM1 antigen. The response of the latter cells, but not the former, to IL-2 is augmented in the presence of macrophages.

Chronic graft-versus-host reaction (GVHR) due to male specific (H-Y) antigen was induced by the injection of syngeneic (DA x Lewis) F1 female cells into (DA x Lewis)F1 male rats. Chronic host-versus-graft reaction (HVGR) based on major histocompatibility complex (MHC) (RT1a) occurred when host Lewis (RT1(1)) rats were transplanted (DA x Lewis)F1 donor cells (RT1a & RT1I). Chronic GVHR and HVGR were activated at fixed periods. The first attacks of the GVHR and HVGR were recognized 50-80 days after cell transplantation, but the most intensive attacks of both responses were observed 120-175 days after cell transplantation. During the most intensive attacks, two rats died from either GVHR or HVGR. Rat immunoglobulin assays measured by radial immunodiffusion (RID) showed that serum IgG2b rose to 10.600-11.500 mg/ml in the rats that had the advanced GVHR or HVGR. The tissue mast cells derived from the loose lymphoid tissues of the medullary and subcapsular sinuses have proliferated in the mesenteric lymph nodes of the rats. IgM and IgG1 binding Fc receptors expressed on the mast cells were demonstrated indirectly using alkaline phosphatase conjugated ant-rat IgM and anti-rat IgG1.

Ten temperature-sensitive (ts) mutants derived from the Edmonston strain of measles virus were characterized by the complementation test and were shown to have four defective sites (A, B, C, and D). Five ts mutants which were confirmed to have a defective site D, induced neither cytopathic effect (CPE) nor an infectious virus. Among the other five ts mutants which produced viral proteins with CPE and showed positive HAD at 39.5 degrees C, the three ts mutants (P253-505, P333, and F2-104) were studied in detail. P253-505 had a defective site C and both P333 and F2-104 had a defective site A. P253-505 and F2-104 produced neither a cell-free nor cell-associated infectious virus and P333 produced only a low level of cell-associated infectious virus. P253-505 and P333 produced virus particles at 39.5 degrees C, while F2-104 did not. The pulse-chase experiment showed a normal pattern of synthesis and processing of viral proteins, but immunofluorescence tests using monoclonal antibodies indicated that P253-505 lacked two epitopes of the M protein at 39.5 degrees C, and both P333 and F2-104 lacked one epitope of the P protein. The lack of these viral epitopes was shown to correlate with the temperature-sensitivity of the three ts mutants.