Search PubMed⌕ Search

Biomedical subjects

K Shimokata

Publications and source records attributed to K Shimokata.

At least 271 records · Page 15Linked to original sources
PubMed1980

Generation and maintenance of immune interferon-producing cells induced by allogeneic stimulation in mice.

When spleen cells derived from C57BL/6 mice immunized with L cells 7 days previously were cocultured with antigenic cells, immune interferon appeared in the culture fluid. We analyzed the tissue distribution of the immune interferon-producing cells (IIPC) which appeared in various lymphoid organs after allogeneic stimulation. Although fluid from cocultures of L-cell-sensitized thymocytes and L-cells could not detect interferon activity consistently, small numbers of IIPC could be detected by using the enumeration method of IIPC. The generation, maintenance, and nature of IIPC emerging in the spleen were different depending on how the host mice were immunized. Multiple antigenic stimulations were more effective and induced longer-lasting immune interferon production than a single stimulation. IIPC induced by a single stimulation appeared to be sensitive to cortisone, vinblastine, and cyclophosphamide and were relatively short lived. In contrast, IIPC induced by multiple stimulations seemed to be partially resistant to these drugs and long lived. When mice were immunized with intact L-cells, carrageenan, a known antimacrophage agent, had no effect on immune interferon production. However, when mice were immunized with solubilized L-cell antigen, this drug displayed a suppressive effect on immune interferon production.

Animals↗
PubMed1979

Protection of mice against virulent virus infection by a temperature-sensitive mutant derived from an HVJ (Sendai virus) carrier culture.

Experimental infection with HVJ (haemagglutinating virus of Japan-the Sendai strain of parainfluenza 1 virus) in mice was studied. Aerosol infection of newborn mice with the wild-type virus (HVJ-W) retarded the development of body weight and killed the animals within a few weeks. Large amounts of virus were isolated from both the lungs and the nasal turbinates of infected mice. In contrast, newborn mice exposed by inhalation to a temperature-sensitive (ts) mutant (HVJ-pB) derived from an HVJ carrier culture showed no clinical signs and grew equally well as mock-infected animals. No infectious virus could be recovered from the lungs although the ts mutant grew to moderate titre in the nasal turbinates. The prior inoculation of newborn mice with the ts mutant virus induced a state of significant resistance to subsequent challenge with the virulent wild-type virus. No replication of challenge virus in both lungs and nasal turbinates could be detected and the animals were protected a lethal infection. It is suggested that an avirulent temperature-sensitive mutant which has lost the capacity to replicate in the lower respiratory tract but is still capable of multiplying in the nasal turbinates may be a promising candidate for use in live vaccines especially against the infectious disease of the lower respiratory tract.

Animals↗
PubMed1979

Interferon susceptibility of various cell lines persistently infected with haemagglutinating virus of Japan (HVJ).

Various cell lines persistently infected with para-influenza 1 virus, HVJ strain, were less susceptible to the antiviral action of interferon than the same cell lines when not infected with HVJ. When Vero cells persistently infected with a temperature-sensitive strain of HVJ were incubated at 38 degrees C, a non-permissive temperature, they became fully susceptible to interferon, whereas neither the haemadsorbing nor the cell-associated haemagglutinating activity of the virus was expressed. These findings suggest that the lowered interferon susceptibility of virus-carrier cells may be related to the maturation of virus in them. It was found that the low susceptibility of virus-carrier cells to interferon is not due to blocked adsorption of interferon or to inability of the cells to respond tointerferon. Studies with actinomycin D suggest that some step (or steps) before the synthesis of the messenger RNA for the antiviral protein is blocked.

Animals↗
PubMed1979

The spread of a pathogenic and an apathogenic strain of Newcastle disease virus in the chick embryo as depending on the protease sensitivity of the virus glycoproteins.

The pathogenic strain Italien and the apathogenic strain Ulster of Newcastle disease virus have been compared with respect to organ tropism and spread of infection in 11-day-old chick embryos. After infection of the endodermal layer of the chorioallantoic membrane by intra-allantoic inoculation with strain Italien, high virus titres are found in all extra-embryonic membranes and fluids and in the embryo itself. Infection results in early death of the embryo. In contrast, after infection with strain Ulster by the same route of inoculation, high virus titres are found only in the allantoic sac and embryos are not killed. Inoculations with strain Italien on to the ectodermal layer through an artificial air sac results in rapid spread of infection in the chorioallantoic membrane and the embryo dies before the virus invades other tissues including the embryo. Under the same conditions of infection, strain Ulster neither spreads within chorioallantoic membrane nor does it kill the embryo. Virus spread in each germinal layer of the chorioallantoic membrane was analysed by immune fluorescence. These studies showed that endoderm as well as mesoderm and ectoderm allowed the spread of strain Italien, whereas only the endoderm is permissive for strain Ulster. These differences in host range are based upon differential activation of the virus glycoproteins by proteolytic cleavage. The glycoproteins of strain Italien are cleaved in each germinal layer, whereas those of strain Ulster are cleaved only in endoderm. These studies demonstrate that, in the system analysed here, spread of infection and organ tropism are important factors for pathogenicity and both of these factors are determined by the susceptibility of the virus glycoproteins to proteolytic cleavage.

Allantois↗
PubMed1979

Immune interferon produced in vitro as a quantitative indicator of cell-mediated immunity.

The present study was constructed to provide some information on the possibility of utilizing immune interferon as a quantitative indicator of cell-mediated immunity and to clarify some of the nature of immune interferon-producing cells (IIPC). When spleen cells derived from L cell-sensitized mice were co-cultivated with L cells, interferon appeared in the culture fluid. It was shown by additional experiments that the cells responsible for immune interferon production in this system were T-lymphocytes assisted by macrophages. The pattern of kinetics of immune interferon production in vitro was similar to that of migration inhibitory factor or T cell-mediated cytotoxicity.

Animals↗
PubMed1979

Examination of latent infection in germfree mice for some murine viruses.

Sera from some groups of germfree mice were examined for reactivity against Sendai, reo 3, Theiler's GD VII, ectromelia, and mouse hepatitis virus antigens. Of 51 sera collected in September and October 1976 and in August and September 1977 from one germfree mouse breeding colony, there was no positive reaction against all the antigens tested. Moreover, the attempt of virus isolation from homogenates of various organs including lungs, liver, kidneys, and intestines of 6 germfree mice was unsuccessful.

Animals↗
PubMed1978

Properties of the viruses selected during persistent infection of L cells with VSV.

Two virus clones, VSV-mp and VSV-sp, were isolated from L cells persistently infected with VSV (New Jersey serotype). Both clones were more temperature sensitive than the parent virus, VSV-o, and grew more slowly, gave smaller plaques, less c.p.e. and lower virus yields in L cells. Unlike the parent virus, both persistent viruses induced interferon production in L cells. Stable carrier cultures could be obtained from L cells infected with VSV-sp at low multiplicities without pretreatment with interferon. This may be related to the fact that VSV-sp is more sensitive to interferon than either VSV-mp or VSV-o.

Cell Fusion↗
PubMed1978

Suppression of interferon production in mouse spleen cells by cytochalasin D.

Cytochalasin D is thought to impair microfilament function. The present study has investigated its effects on four different systems in which interferon is formed, namely (1) mouse fibroblasts induced with virus (2) mouse spleen cells induced with virus, or (3) with endotoxin or (4) by allogeneic stimulation. Cytochalasin D did not suppress formation of interferon by fibroblasts (L cells) or spleen cells stimulated with either HVJ or NDV. However it did suppress production of interferon by spleen cells in response to endotoxin or an allogeneic stimulation; here its action was apparently not on the secretion of interferon, but on some earlier event. It also suppressed the production of interferon by mouse spleen cells induced with HVJ if this had been u.v. irradiated for more than 15 min: this suggests that cytochalasin D sensitive structures do play some role in interferon production by mouse spleen cells when stimulated with HVJ, as well as when they are stimulated with endotoxin or an allogeneic stimulus.

Antigen-Antibody Reactions↗
PubMed1978

Studies on the pathogenicity of human-origin parainfluenza virus in the brain of mice.

The pathogenicity of parainfluenza type 2 (croup-associated) virus known to cause infections of the respiratory tract in the early life of man was studied in the brain of mice. One- to 4-day-old sucklings and 4-week-old mice were inoculated intracerebrally with the virus. The virus multiplied in sucklings, but not in adults. Most mice inoculated intracerebrally with the virus appeared healthy. Histological examination showed minimum inflammatory changes, although moderate hydrocephalus developed in three of twenty-one sucklings by 6 weeks post-infection. Immunofluorescent study in sucklings showed viral antigens in ependymal lining cells and choroid plexus epithelium during the first two weeks, and parenchymal cells for more than two months. Virus specific antibody response was observed in adults, but not in sucklings. One interesting finding was that viral antigens persisted in six out of 11 suckling brains for one to two months.

Animals↗
PubMed1977

Comparative studies on cytopathic effects induced by vesicular stomatitis virus in two cell types.

Infection of mouse L cells with vesicular stomatitis virus (VSV) leads to an extensive cell fusion, while porcine kidney stable (PS) cells infected with VSV show only cell rounding. Therefore, comparative morphological studies on the infection of the two cell lines were carried out using a transmission or scanning electron microscope and an immunofluorescence microscope. PS cells infected with VSV contrasted to L cells infected with the same virus in the following two points; (1) the principal site of VSV maturation was the intracytoplasmic vacuolar membrane in PS cells and the plasma membrane in L cells. However, it was found that viral glycoprotein was present on the cell surface of infected PS cells; (2) the morphological changes at the cell surface of infected PS cells occurred much earlier and were severer than those at the cell surface of infected L cells. From these observations, we discuss the possibility that the surfaceembrane of PS cells is too sensitive to the VSV-induced cell damage to cause cell fusion.

Animals↗
PubMed1977

Affinity of Sendai virus for the inner ear of mice.

The direct immunofluorescent antibody method revealed that Sendai virus, which was thought to be most prevalent in respiratory diseases in mice, infected the inner ear of mice when the virus was injected intracerebrally. Specific immunofluorescence that indicated the presence of antigens of Sendai virus was observed in both perilymphatic and endolymphatic structures. The routes of virus spread are discussed. This experimental study, using newborn mice and Sendai virus, may be useful for the investigation of the pathogenesis of viral labyrinthitis not only because of the high frequency of inner ear infection, but also because of long-time survivors which facilitate prolonged observation.

Animals↗
PubMed1976

Relationship between establishment of persistent infection of haemagglutinating virus of Japan and the properties of the virus.

The infectious virus (HVJ-pi) obtained from BHK cells persistently infected with haemagglutinating virus of Japan was found to be temperature-sensitive as well as causing little or no cytopathic effect (c.p.e.) and leading to establishment of carrier cultures in several cell lines at both permissive (32 degrees C) and non-permissive (38 degrees C) temperature. In order to obtain information about the role of HVJ-pi in the establishment of persistent infection, comparative studies were made of some phenotypic properties of HVJ-pi and HVJ-38 which was obtained by passing wild-type HVJ in eggs at 38 degrees C and was proved to be highly cytopathic. HVJ-pi differed from HVJ-38 in (1) temperature sensitivity in its ability to produce virus progeny, (2) infectivity for embryonated eggs, (3) neuraminidase activity, (4) the thermal stability of HA and neuraminidase activity, and (5) the polypeptide composition of BHK-grown viruses. B cells infected with HVJ-pi release haemagglutinin more efficiently, and less HA was accumulated on the cell membrane. In considering these results, it was concluded that the difference of envelope proteins might be involved in the striking difference in c.p.e. between HJV-pi and HVJ-38.

Cell Line↗
PubMed1976

Polykaryocyte formation induced by VSV in mouse L cells.

Infection of mouse L cells with VSV leads to the formation of polykaryocytes about 4 to 12 h p.i. When anti-VSV immune serum was added during the course of infection, progression of cell fusion was soon suppressed. Cycloheximide completely suppressed the cell fusion when the drug was added within 1 h p.i., while the cell fusion was not suppressed at all when the drug was added at and after 3 h. Early polykaryocyte formation, 'fusion from without', was observed only at a low level in cells infected at very high multiplicities. The development of cell fusion induced by VSV was found to be different in several cell types, although all these cells produced a rather high yield of virus: L and C-243-3 mouse cell lines showed a high level of polykaryocytosis (80 to 100%), BHK and RK-13 cells responded at low level, and PS and Vero cells showed no cell fusion in response to VSV infection. In PS cells, however, cell fusion occurred when VSV-infected L cells were co-cultivated. From these observations, the mechanism of cell fusion induced by VSV was discussed.

Animals↗