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Biomedical subjects

H Fujisawa

Publications and source records attributed to H Fujisawa.

At least 343 records · Page 19Linked to original sources
PubMed1987

Mechanism of protection during the early phase of a generalized viral infection. II. Contribution of polymorphonuclear leukocytes to protection against intravenous infection with influenza virus.

The contribution of phagocytes to the early protection of mice inoculated intravenously with influenza virus was investigated in phagocyte-depleted mice. Following the inoculation of a sublethal dose of influenza virus, virus titres in the liver and lung of both untreated and carrageenan-treated mice were reduced rapidly by day 1 and decreased slowly to reach an undetectable level by day 7. The titres in gamma-irradiated mice decreased transiently by day 1 and increased progressively thereafter to kill all of the hosts by day 8. The clearance of virus from blood at the early stage of infection was retarded by gamma-irradiation but not by carrageenan treatment. In addition, increase in virus titres in the liver and lung in the early stage of the infection was prevented by adoptive transfer with syngeneic polymorphonuclear leukocytes into gamma-irradiated mice. No significant rise of neutralizing antibody was detectable by day 3 after the inoculation, in any of the three groups of mice. These observations imply that gamma-sensitive and carrageenan-resistant polymorphonuclear leukocytes play a protective role at the early stage in the infection, whereas fixed macrophages or natural killer cells, both of which are carrageenan-sensitive and gamma-resistant, scarcely participate in the early phase.

Animals↗
PubMed1987

Protective mechanisms against pulmonary infection with influenza virus. I. Relative contribution of polymorphonuclear leukocytes and of alveolar macrophages to protection during the early phase of intranasal infection.

The relative contribution of polymorphonuclear leukocytes and macrophages in the early protection against intranasal infection of mice with influenza virus was investigated. Virus multiplication in the lung in the early phase of infection with less than 1.5 X 10(3) plaque-forming units was enhanced by X-ray irradiation. The intranasal administration of carrageenan did not influence the titre of virus. However, when mice were infected with 1.5 X 10(4) plaque-forming units, the virus titre was elevated by intranasal administration of carrageenan as well as by X-ray irradiation, but not by intraperitoneal administration of carrageenan. The intranasal administration of carrageenan not only inhibited the phagocytic activity of alveolar macrophages but also enhanced susceptibility to the virus. On the other hand, polymorphonuclear leukocytes were capable of phagocytosing the virus in vitro and were non-permissive for virus infection. Neutralizing antibody and interferon were not detectable in the early stage of the infection. These results suggested that polymorphonuclear leukocytes (X-ray-sensitive, carrageenan-resistant) were the cells primarily responsible for early protection in influenza virus infection and that after infection with a high dose of the virus alveolar macrophages (X-ray-resistant, carrageenan-sensitive) also played a protective role in the early phase.

Administration, Intranasal↗
PubMed1987

Oral immunization in adult mice to live and heat-killed Vibrio cholerae.

Effects of systemic and intestinal local immune responses in mice fed ad libitum and forcedly with live or heat-killed Vibrio cholerae on the elimination of vibrios from the intestine were investigated. In mice fed with live vibrios, ad libitum feeding could induce potential delayed-type hypersensitivity and rapid production of vibriocidal antibody in the serum whereas forcedly feeding suppressed the delayed-type hypersensitivity and retarded the antibody production. In contrast, when killed microorganisms were used as antigens, significant delayed-type hypersensitivity and rapid response of vibriocidal antibody were induced in forcedly fed mice although ad libitum feeding suppressed the induction of the delayed-type hypersensitivity and retarded the production of vibriocidal antibody. The elimination of vibrios from the intestine of mice was promoted in both mice groups fed ad libitum and forcedly with live vibrios but not with killed microorganisms. Total IgA in the intestinal contents of mice fed with live vibrios both ad libitum and forcedly were higher than those of mice fed with killed antigens. In addition, when the extracts of intestinal contents were absorbed by live antigens, IgA contents in mice fed with live vibrios were reduced more markedly than those in mice immunized orally by the feeding with killed antigens. These findings suggested that the elimination of vibrios from the organ was closely related to local IgA antibody response to heat-labile substance of live Vibrio cholerae.

Animals↗
PubMed1987

Immunohistochemical characterization of rat pineal dopamine beta-hydroxylase-containing structures: use of a homologous monoclonal antibody.

Previous immunohistochemical studies using a polyclonal heterologous antibody to dopamine-beta-hydroxylase (DBH) (EC 1.14.17.1) have shown that only a few of the many sympathetic nerve fibers in the rat pineal display DBH-like immunoreactivity. This is in contrast to other sympathetically innervated organs. To ascertain this observation and to rule out antibody- or method-related artifacts, in the present study a well-characterized, monospecific, homologous monoclonal antibody to DBH was used in combination with the biotin-streptavidin-fluorescein-mediated detection system. As in a previous study, immunoreactive fibers were only rarely encountered in the rat pineal gland, with an identical distribution pattern. The present findings indicate that the sympathetic nerve fibers in the rat pineal gland appear to have a low capacity for de novo synthesis of noradrenaline and that most of the noradrenaline present may be taken up from the general circulation. In addition to nerve fibers, perikarya-like cells and endbulb-like structures were seen in the pineal gland similar to those demonstrated by the polyclonal antibody. It is suggested that both structures may be part of an as yet unknown intrapineal regulatory system.

Animals↗
PubMed1987

Cholera toxin-induced tolerance to allografts in mice.

When C3H/HeN (C3H) mice were primed with viable C57BL/6 (B6) spleen cells and treated with cholera toxin (CT) on the same day, a profound tolerance to tumour allografts of B6 origin was induced. The tolerant state was sustained for as long as 6 weeks or more. Skin allografts of B6 were rejected by such tolerant C3H mice, although the survival times were prolonged very slightly. Generation of cytotoxic T lymphocytes was reduced markedly in the tolerant mice, whereas delayed footpad reaction to B6 cells was maintained at the normal immune level or higher. There is a possibility that a T-cell subset responsible for delayed footpad reaction is resistant to CT-induced tolerance and participates in the rejection of skin allografts in tolerant mice.

Animals↗
PubMed1987

Contradictory responses in induction of delayed type hypersensitivity in orally immunized mice.

Induction of delayed type hypersensitivity (DTH) in mice fed with sheep red blood cells (SRBC) and live Vibrio cholerae (V. cholerae) both forcedly and ad lib was comparatively investigated. Although suppression of DTH to SRBC or V. cholerae was induced in mice fed forcedly for 1 or 2 weeks, mice fed ad lib could produce the positive footpad reactions to antigens. Furthermore, the suppression of DTH in forcedly fed mice showed an antigenic specificity. These observations indicated that the induction of unresponsiveness to DTH in orally immunized mice was markedly influenced by the oral administration.

Administration, Oral↗
PubMed1987

Enhancement of host defence by Y-19995 (2,4'-bis(1-methyl-2-dimethyl-aminoethoxyl)-3-benzoylpyridine dimaleate), a novel synthetic compound. I. Accelerated restoration from the leukocytopenia and augmented protection against microbial infections in immunocompromised mice.

Effects of a novel synthetic compound, Y-19995, on the host defence in immunocompromised mice were investigated in terms of the restoration of leukocytopenia and the protection against several microbial infections. Oral or intravenous administration of Y-19995 into mice after X-irradiation, treatment with cyclophosphamide or mitomycin C prevented the leukocytopenia to some extent and promoted the restoration in cell numbers of both the peripheral blood leukocytes and bone marrow. Intravenous administration of Y-19995 increased significantly the survival rates of X-ray irradiated mice against acute systemic infections with Escherichia coli, Pseudomonas aeruginosa and Candida albicans, and intramuscular infection with Escherichia coli. The clearance of Escherichia coli from the blood of X-ray irradiated mice was also promoted by the treatment with Y-19995. The augmented protection against microbial infections in immunocompromised hosts by Y-19995 may be attributed mainly to the prevention of leukocytopenia or the enhanced restoration from leukocytopenia.

Animals↗
PubMed1987

Enhancement of host defence by Y-19995 (2,4'-bis(1-methyl-2-dimethyl-aminoethoxyl)-3-benzoylpyridine dimaleate), a novel synthetic compound. II. Activation of phagocytic cell functions.

A novel synthetic compound, Y-19995 potentiated phagocytic activity of rat or mouse peritoneal polymorphonuclear leukocytes in vitro or in vivo, respectively. The agent enhanced NBT reducing capacities of rat and guinea pig polymorphonuclear leukocytes in the peripheral blood ex vivo. Y-19995 restored from phagocytic activity of mouse peritoneal macrophages suppressed by the treatment with prednisolone ex vivo. In addition, IL-1 production by mouse macrophages was augmented by culturing with the agent in vitro. Furthermore, Y-19995 potentiated both phagocytic activity and NBT reducing capacity of human peripheral polymorphonuclear leukocytes in vitro. These results suggested that the activation of phagocytic cell functions by Y-19995 contributed to the enhancement of host defence in immunocompromised hosts.

Adjuvants, Immunologic↗
PubMed1987

Differing resistance to polymorphonuclear cells of halophilic- and hypotonic-types of Vibrio vulnificus.

Bacterial growth and lethality of 4 strains of Vibrio vulnificus infection of mice were enhanced by gamma-irradiation but not by treatment with carrageenan. Therefore, protection against V. vulnificus, at least in the early phases, probably depends mainly on polymorphonuclear cells (PMN), since carrageenan depletes macrophages but not PMN. PMN dependent protection against infection differs for 2 types of V. vulnificus strains. Halophilic- and hypotonic-type were distinguished from the corresponding parent strain. The hypotonic-type of the strains had capsular materials, as clarified by electron microscopic observation of the organisms stained with ruthenium red. On the other hand, halophilic-types either had no observable capsular materials, or incomplete materials, in contrast to the corresponding hypotonic-type. The corresponding halophilic- and hypotonic-types of the strains were compared for virulence in mice. The strains with capsular materials acquired resistance to phagocytic activity and were highly lethal. Capsular materials of V. vulnificus are no doubt important for the expression of virulence.

Animals↗
PubMed1986

Further comparison of calmodulin-dependent protein kinase II from brain and calmodulin-dependent glycogen synthase kinase from skeletal muscle.

Calmodulin-dependent protein kinase II was purified from rabbit brain and its properties were compared with those of calmodulin-dependent protein kinase II from rat brain and calmodulin-dependent glycogen synthase kinase from rabbit skeletal muscle. Rabbit brain calmodulin-dependent protein kinase II was clearly distinguished from rabbit skeletal muscle glycogen synthase kinase with respect to size, behavior on autophosphorylation, immunological cross-reactivity and peptide mapping, but was indistinguishable from rat brain calmodulin-dependent protein kinase II in all respects examined. Thus, differences between calmodulin-dependent protein kinase II and glycogen synthase kinase appear not to reflect a species difference but to reflect a tissue difference.

Animals↗