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Biomedical subjects

M Homma

Publications and source records attributed to M Homma.

At least 253 records · Page 14Linked to original sources
PubMed1986

The functions of oligosaccharide chains associated with influenza C viral glycoproteins. I. The formation of influenza C virus particles in the absence of glycosylation.

The effect of a glycosylation inhibitor, tunicamycin (TM) on the replication of influenza C virus was investigated. Incorporation of [3H]-glucosamine into the gp88 glycoproteins of this virus was completely inhibited by TM at the concentrations higher than 0.25 microgram/ml. Under these conditions, the synthesis of internal proteins NP and M was shown in TM-treated cells but the synthesis of gp88 was not. The disappearance of gp88 was however accompanied with the appearance of two new polypeptides with molecular weights of 80,000 (T80) and 76,000 (T76). While T80 was identified by peptide mapping as a host cell protein whose synthesis was enhanced by TM, T76 was shown to correspond to a nonglycosylated form of gp88. Pulse-chase experiments revealed that there was no significant difference in the intracellular stability of T76 and gp88. Although TM depressed the production of infectious progeny virus greater than 100-fold, only a five-fold decrease was observed in the release of noninfectious physical particles, suggesting that glycosylation is not essential for the formation of influenza C virus particles. However, the virions from TM-treated cells had a lower buoyant density in isopycnic sucrose gradients and lacked surface proteins in either glycosylated or nonglycosylated form.

Amnion↗
PubMed1986

The functions of oligosaccharide chains associated with influenza C viral glycoproteins. II. The role of carbohydrates in the antigenic properties of influenza C viral glycoproteins.

The antigenic properties of influenza C viral glycoprotein gp88 were compared with those of its nonglycosylated counterpart T76 synthesized in infected cells treated with tunicamycin. Radioimmunoprecipitation experiments with three different monoclonal antibodies against gp88 revealed that an antibody designated Q-5 precipitated gp88 but not T76, indicating the requirement for glycosylation for the binding of this antibody to gp88. It is unlikely, however, that the antigenic determinant recognized by Q-5 is carbohydrate moiety since the ability of the antibody to bind to gp88 varied depending on the virus strain, and trypsin-treatment of gp88 eliminated its reactivity with Q-5. Gel electrophoretic analysis under nonreducing conditions showed that T76 underwent the formation of disulfide-linked multimers in the absence of reducing agent while gp88 behaved as monomers, suggesting that glycosylation is required for gp88 molecules to attain an appropriate conformation. These observations, altogether, suggests that glycosylation is important in determining the immunological specificity of gp88 presumably by influencing the folding of this glycoprotein.

Amnion↗
PubMed1986

Genetic variation among human strains of influenza C virus isolated in Japan.

The RNA genomes of sixteen human strains of influenza C virus isolated in Japan between 1964 and 1983 were compared by SDS-polyacrylamide gel electrophoresis and oligonucleotide fingerprinting. A high degree of genetic variation was observed among the strains analysed. However, there were some strains with the genomes closely related to one another, and they could be divided into two groups. The first group consists of C/Shizuoka/79, C/Kanagawa/1/81 and four strains of C/Yamagata/81. The 1981 strains of this group were all isolated in March of the year. The second one consists of C/Kyoto/41/82, C/Nara/82 and C/Hyogo/1/83 that were isolated between February 1982 and December 1983. Little or no difference was observed in the genomes of the same group, while the difference was evident between two groups. The Aichi/1/81 strain isolated in November 1981 had a genome distantly related to either of these two groups. Thus three different types of influenza C virus were isolated during the period of 12 mth from March 1981 to February 1982, suggesting that multiple influenza C viruses with distant genetic relationship were circulating at the same time in Japan.

Animals↗
PubMed1986

In vitro reconstitution of flagellar filaments onto hooks of filamentless mutants of Salmonella typhimurium by addition of hook-associated proteins.

An in vitro system for reconstituting flagellar filaments onto hooks of filamentless mutants of Salmonella typhimurium was used to investigate the role played in filament formation by the three hook-associated proteins (HAPs, products of the flaW, flaU, and flaV genes). These proteins--FlaW, FlaU, and FlaV--are believed to be assembled in this order at the distal end of the hook. When the recipient hooks were provided by flaU mutants, whose hook tips contained FlaW only, exogenous FlaU was essential for polymerization of both exogenous and endogenous flagellin, whereas exogenous FlaV inhibited such polymerization. When the recipients were flaV-mutant hooks, whose tips contained FlaW and FlaU but not FlaV, exogenous FlaV inhibited polymerization of exogenous flagellin. FlaV also inhibited polymerization of exogenous flagellin at the tips of filament fragments. In contrast, FlaV was essential for polymerization of endogenous flagellin onto flaV-mutant hooks, and onto short filaments that had been made (in the absence of FlaV) by polymerization of exogenous flagellin on the tips of flaV-mutant hooks. These results suggest that FlaV acts not only at the tip of the hook to initiate growth of the filament, but also at the tip of the growing filament, and that FlaV is essential for polymerization of endogenous flagellin--i.e., for the normal process of filament assembly in vivo.

Bacterial Proteins↗
PubMed1986

Experimental infections of dogs with type C influenza virus.

A study was performed to determine if type C influenza infection could be established in dogs as a model for human cases. Mongrel dogs were infected with the Ann Arbor/1/50 strain of type C influenza virus and were examined for clinical symptoms, virus isolation and antibody response. After the first exposure to the virus, all infected animals developed nasal discharge and some of them also showed swelling of the eyelids, and suffusion of the eyes with tears and eye mucus, within 1 to 4 days. The animals showed an increase in hemagglutination-inhibiting (HI) serum antibody, and recovery of the agent from the nasal swabs was successful. The symptoms lasted for as long as 10 days in most infected dogs, which was comparable to our human cases reported previously (Katagiri, S., Ohizumi, A., and Homma, M. 1983. J. Infect. Dis. 48: 51-56). After the second and third virus exposures at intervals of 50 days, all animals developed the same symptoms as those described above and the rise in antibody titer was evident. The virus could be recovered from four of the six dogs 2 to 5 days after the second exposure and from one dog as late as 10 days after the third exposure. Increases in antibody titer in the IgM fraction were observed after every infection. In control dogs which were mock-infected with UV-inactivated virus, no symptoms were evident and recovery of the virus was not successful although an increase in HI serum antibody titer was seen. These results show that mongrel dogs are sensitive to type C influenza virus and that repeated infections characteristic of human influenza C can be experimentally produced in dogs.

Animals↗
PubMed1986

Degranulation and histamine release from murine mast cells sensitized with dengue virus-immune sera.

Mice were immunized with dengue type 2 virus (DEN 2) under a schedule favoring the production of IgE antibody. The antibody obtained could sensitize peritoneal resident mast cells both in vitro and in vivo so that the sensitized cells were degranulated and released histamine on challenge with the DEN 2 antigen. It was also demonstrated that the antibody was cytophilic and heat-labile. The above observations suggest that the present experimental system can be used to detect anti-DEN 2 IgE antibody in mice.

Animals↗
PubMed1986

Direct demonstration of immunoregulatory T-cell defects in patients with systemic lupus erythematosus.

The present study was undertaken to determine directly whether immunoregulatory T cells have a defective suppressor function in patients with systemic lupus erythematosus (SLE), and whether anti-T-cell antibodies are essential for immunoregulatory T-cell defects. Peripheral blood T cells and T-cell subsets were determined in 52 SLE patients. The ratio of T4 to T8 cells was distributed over a wider range in patients with SLE than in the controls. Patients with SLE were divided into three groups (low, normal and high) by the T4/T8 ratio. Lymphocytes from 12 SLE patients (7 with low and 5 with high T4/T8 ratios) were studied extensively. Their disease was inactive or in remission. Anti-T-cell antibodies were not detected, and yet the patients had immunological abnormalities characterized by the presence of antinuclear antibodies and hypergammaglobulinaemia. The SLE patients with high T4/T8 ratios had a decreased number of T8 cells, and defective suppressor-effector cells. In contrast, patients with low T4/T8 ratios had decreased T4 cells and/or increased T8 cells, and defective suppressor-inducer cells. Two patients with low T4/T8 ratios had both suppressor-effector and suppressor-inducer cell defects. These results indicate that immunoregulatory circuits in SLE patients are heterogeneous and that immunoregulatory defects exist even when the disease is inactive or in remission. Anti-T-cell antibodies were not essential for such immunoregulatory defects. Thus, immunoregulatory T-cell defects and the development of SLE may be independent conditions due to other unknown causes.

Adult↗
PubMed1986

Isolation of an antigenically unique methanogen from human feces.

A methanogenic bacterium with the morphological and physiological properties of the genus Methanobrevibacter was isolated from the feces of a Japanese man who excreted methane in his breath. Indirect immunofluorescence staining revealed that the isolate had an antigenicity unrelated to that of any known members of the genus Methanobrevibacter.

Antigen-Antibody Complex↗
PubMed1986

Changes in bronchial reactivity to acetylcholine with type C influenza virus infection in dogs.

To investigate the mechanisms involved in increasing bronchial reactivity, we made a model of airway reactivity increase in dogs after Type C influenza virus infection. Five beagle dogs were inoculated intranasally with the virus, and the time courses of changes in the hemagglutination inhibition (HI) antibody titer and the bronchial reactivity were determined. To assess bronchial reactivity the dogs were anesthetized, and dose-response curves of pulmonary resistance were obtained against increasing concentrations of acetylcholine aerosol. The dogs infected with the virus showed mild symptoms of rhinorrhea and cough. The HI antibody titer was significantly increased in all dogs, with peak values at 1 to 3 wk after infection. The bronchial reactivity to acetylcholine began to increase towards Day 3, reached a peak at 1 to 2 wk, and returned to a normal level at 4 wk. The airway reactivity to acetylcholine at 2 wk after infection was increased by 2.3 to 6.5 times the normal value in terms of the acetylcholine provocative concentration. The mean increase was significant at 1 wk (p less than 0.05), 2 wk (p less than 0.01), and 3 wk (p less than 0.05). Although both the HI antibody titer and the airway responsiveness increased together towards 1 to 2 wk, no close relationship between these factors was observed thereafter. The present dog model of airway hyperreactivity may be useful for further investigation of the mechanism governing increase in bronchial reactivity with respiratory viral infection in normal subjects as well as in patients with asthma.

Acetylcholine↗
PubMed1986

Effects of alpha-macroglobulins and murinoglobulins on the hemagglutination by influenza C virus.

Rat alpha-1- and alpha-2-macroglobulins as well as rat murinoglobulins I and II were shown to inhibit hemagglutination by influenza C virus. In marked contrast, neither alpha-macroglobulins nor murinoglobulins from mouse or guinea pig plasma had the inhibitory activity. These results suggest that the hemagglutination-inhibiting activity of rat alpha-macroglobulins or murinoglobulins is not related to their protease-binding capacity.

Animals↗
PubMed1986

Antibody-mediated enhancement of infection by dengue virus of the P815 murine mastocytoma cell line.

Dengue type 2 virus (DEN 2) could replicate only to a limited extent in a murine mastocytoma cell line, P815. The viral multiplication was enhanced 10- to 100-fold by mouse anti-DEN 2 antiserum or anti-DEN 2 type-specific monoclonal antibody diluted beyond their neutralizing titers. Cells incubated with virus-antibody mixtures changed morphologically, developing a mature mast cell-like appearance, 4-5 days after infection. The indirect fluorescent antibody technique showed that the enhancement of infection was caused by an increase in the number of DEN 2-infected cells. This is the first report that cells of mast cell lineage support dengue virus multiplication, and that virus production is enhanced in the presence of anti-dengue antibodies.

Animals↗
PubMed1986

Anti-Ro/SSA and -La/SSB antibodies in patients with connective tissue diseases.

The frequency of anti-Ro/SSA and anti-La/SSB antibodies in patients from Japan with Sjögren's syndrome, systemic lupus erythematosus (SLE), progressive systemic sclerosis (PSS), polymyositis-dermatomyositis (PM-DM), rheumatoid arthritis (RA) and blood donors is reported. Anti-La/SSB ab was especially detected in patients with severe glandular and extraglandular manifestation and could be found in sera years prior to the confirmation of Sjögren's syndrome. The purified Ro/SSA antigen consisted of 60 k peptide and 16 k RNA while the La/SSB antigen consisted of 41 k and 29 k peptides. Some molecular association seems to exist between the peptides and corresponding IgG anti-Ro/SSA and anti-La/SSB antibodies.

Antibodies, Antinuclear↗
PubMed1985

Suppression of rheumatoid factor synthesis by antiidiotypic antibody in rheumatoid arthritis patients with cross-reactive idiotypes.

The effect of antiidiotypic antibody on the in vitro production of rheumatoid factor was studied in rheumatoid arthritis patients with cross-reactive idiotypic determinants. Antiidiotypic antibodies (ascites IgG) were developed against monoclonal rheumatoid factor (Ka m-RF) by a cell fusion procedure. These antibodies were idiotype-specific, since: 1) they reacted only with F(ab')2 fragment of Ka m-RF; 2) they failed to react with normal IgM without rheumatoid factor activity; and 3) their F(ab')2 fragment inhibited the rheumatoid factor activity of Ka m-RF. The antiidiotypic antibody strongly suppressed the in vitro production of rheumatoid factor by lymphocytes from unrelated rheumatoid arthritis patients with cross-reactive idiotypes. The suppression was specific, since ascites IgG failed to suppress in vitro anti-keyhole limpet hemocyanin antibody production by the lymphocytes. These results indicate that antiidiotypic antibody may influence the regulation of rheumatoid factor production in patients with rheumatoid arthritis.

Antibodies, Monoclonal↗
PubMed1985

Isolation and characterization of influenza C virus inhibitor in rat serum.

Two hemagglutination inhibitors for influenza C virus were isolated from pooled sera of normal rats by sequential chromatography on Blue Sepharose CL 6B, Ultrogel AcA 22, and DEAE-cellulose. The two inhibitors were identified as alpha 1-macroglobulin and murinoglobulin by comparison with the authentic samples. These inhibitors abolished the hemagglutination by influenza C virus strains but did not affect the hemagglutination by influenza A and B virus strains. Hemagglutination inhibition activity of both inhibitors was completely destroyed by incubation with influenza C virus at 37 degrees C but not with the other types of influenza virus, indicating that the inhibitors are specific for influenza C virus. The inhibitory activity was also destroyed by incubation with neuraminidase from Arthrobacter ureafaciens. By contrast, no activity was lost after treatment with neuraminidase from Vibrio cholerae. These results suggest that the sialic acid residue(s) which is cleavable by the former neuraminidase but not by the latter is essential for the hemagglutination inhibition. The two inhibitors were inactivated by treating with sodium hydroxide and methylamine but not with sodium metaperiodate.

Animals↗
PubMed1985

Isolation and characterization of influenza C virus inhibitors in rat serum.

Two inhibitors against haemagglutination by influenza C virus were isolated from pooled sera of normal rats by sequential chromatography on Blue Sepharose CL 6B, Ultrogel AcA 2, and DEAE-cellulose. The two inhibitors were identified as alpha 1-macroglobulin and murinoglobulin by comparison with the authentic samples. These inhibitors abolished the haemagglutination by influenza C virus strains but did not affect the haemagglutination by influenza A and B virus strains. Haemagglutination inhibition activity of both inhibitors was completely destroyed by incubation with neuraminidase from Arthrobacter ureafaciens. By contrast, no activity was lost after treatment with neuraminidase from Vibrio cholerae. These results suggest that the sialic acid residue(s) which is excised by the former neuraminidase but not by the latter is essential for the haemagglutination inhibition. The two inhibitors were inactivated by treating with sodium hydroxide and methylamine but not with sodium metaperiodate.

Animals↗