12 results on '"Shimohigoshi M"'
Search Results
2. Development of Photocatalyst Tile and Commercial Production
- Author
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Shimohigoshi, M., primary
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- 2005
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3. Contact Angle and Boiling Heat Transfer of TiO_2-sputtered Surface
- Author
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Takata, Y., primary, Hidaka, S., additional, Cao, J. M., additional, Masuda, M., additional, Ito, T., additional, Watanabe, T., additional, and Shimohigoshi, M., additional
- Published
- 2000
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4. Development of uric acid and oxalic acid sensors using a bio-thermochip
- Author
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Shimohigoshi, M. and Karube, I.
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- 1996
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5. Development of a bio-thermochip and its application for the detection of glucose in urine
- Author
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Shimohigoshi, M., Yokoyama, K., and Karube, I.
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- 1995
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6. The development of calorimetric biosensors using chip thermistors
- Author
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Shimohigoshi, M., Yokoyama, K., Tamiya, E., and Karube, I.
- Published
- 1994
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7. An enterococcal phage-derived enzyme suppresses graft-versus-host disease.
- Author
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Fujimoto K, Hayashi T, Yamamoto M, Sato N, Shimohigoshi M, Miyaoka D, Yokota C, Watanabe M, Hisaki Y, Kamei Y, Yokoyama Y, Yabuno T, Hirose A, Nakamae M, Nakamae H, Uematsu M, Sato S, Yamaguchi K, Furukawa Y, Akeda Y, Hino M, Imoto S, and Uematsu S
- Subjects
- Adult, Aged, Animals, Female, Humans, Male, Mice, Middle Aged, Young Adult, Biofilms drug effects, Biofilms growth & development, Dysbiosis complications, Dysbiosis microbiology, Feces microbiology, Germ-Free Life, Hematopoietic Stem Cell Transplantation adverse effects, In Vitro Techniques, Intestines drug effects, Intestines microbiology, Perforin metabolism, Risk Factors, Transplantation, Homologous adverse effects, Whole Genome Sequencing, Drug Resistance, Bacterial drug effects, Anti-Bacterial Agents pharmacology, Bacteriophages enzymology, Bacteriophages genetics, Enterococcus faecalis drug effects, Enterococcus faecalis genetics, Enterococcus faecalis growth & development, Enterococcus faecalis metabolism, Enterococcus faecalis virology, Gastrointestinal Microbiome, Graft vs Host Disease complications, Graft vs Host Disease microbiology, Graft vs Host Disease prevention & control, Graft vs Host Disease therapy
- Abstract
Changes in the gut microbiome have pivotal roles in the pathogenesis of acute graft-versus-host disease (aGVHD) after allogenic haematopoietic cell transplantation (allo-HCT)
1-6 . However, effective methods for safely resolving gut dysbiosis have not yet been established. An expansion of the pathogen Enterococcus faecalis in the intestine, associated with dysbiosis, has been shown to be a risk factor for aGVHD7-10 . Here we analyse the intestinal microbiome of patients with allo-HCT, and find that E. faecalis escapes elimination and proliferates in the intestine by forming biofilms, rather than by acquiring drug-resistance genes. We isolated cytolysin-positive highly pathogenic E. faecalis from faecal samples and identified an anti-E. faecalis enzyme derived from E. faecalis-specific bacteriophages by analysing bacterial whole-genome sequencing data. The antibacterial enzyme had lytic activity against the biofilm of E. faecalis in vitro and in vivo. Furthermore, in aGVHD-induced gnotobiotic mice that were colonized with E. faecalis or with patient faecal samples characterized by the domination of Enterococcus, levels of intestinal cytolysin-positive E. faecalis were decreased and survival was significantly increased in the group that was treated with the E. faecalis-specific enzyme, compared with controls. Thus, administration of a phage-derived antibacterial enzyme that is specific to biofilm-forming pathogenic E. faecalis-which is difficult to eliminate with existing antibiotics-might provide an approach to protect against aGVHD., (© 2024. The Author(s).)- Published
- 2024
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8. Prime-boost-type PspA3 + 2 mucosal vaccine protects cynomolgus macaques from intratracheal challenge with pneumococci.
- Author
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Yokota C, Fujimoto K, Yamakawa N, Kono M, Miyaoka D, Shimohigoshi M, Uematsu M, Watanabe M, Kamei Y, Sugimoto A, Kawasaki N, Yabuno T, Okamura T, Kuroda E, Hamaguchi S, Sato S, Hotomi M, Akeda Y, Ishii KJ, Yasutomi Y, Sunami K, and Uematsu S
- Abstract
Background: Although vaccination is recommended for protection against invasive pneumococcal disease, the frequency of pneumococcal pneumonia is still high worldwide. In fact, no vaccines are effective for all pneumococcal serotypes. Fusion pneumococcal surface protein A (PspA) has been shown to induce a broad range of cross-reactivity with clinical isolates and afford cross-protection against pneumococcal challenge in mice. Furthermore, we developed prime-boost-type mucosal vaccines that induce both antigen-specific IgG in serum and antigen-specific IgA in targeted mucosal organs in previous studies. We investigated whether our prime-boost-type immunization with a fusion PspA was effective against pneumococcal infection in mice and cynomolgus macaques., Methods: C57BL/6 mice were intramuscularly injected with fusion PspA combined with CpG oligodeoxynucleotides and/or curdlan. Six weeks later, PspA was administered intranasally. Blood and bronchoalveolar lavage fluid were collected and antigen-specific IgG and IgA titers were measured. Some mice were given intranasal Streptococcus pneumoniae and the severity of infection was analyzed. Macaques were intramuscularly injected with fusion PspA combined with CpG oligodeoxynucleotides and/or curdlan at week 0 and week 4. Then, 13 or 41 weeks later, PspA was administered intratracheally. Blood and bronchoalveolar lavage fluid were collected and antigen-specific IgG and IgA titers were measured. Some macaques were intranasally administered S. pneumoniae and analyzed for the severity of pneumonia., Results: Serum samples from mice and macaques injected with antigens in combination with CpG oligodeoxynucleotides and/or curdlan contained antigen-specific IgG. Bronchial samples contained antigen-specific IgA after the fusion PspA boosting. This immunization regimen effectively prevented S. pneumoniae infection., Conclusions: Prime-boost-type immunization with a fusion PspA prevented S. pneumoniae infection in mice and macaques., (© 2023. The Author(s).)
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- 2023
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9. Functional Restoration of Bacteriomes and Viromes by Fecal Microbiota Transplantation.
- Author
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Fujimoto K, Kimura Y, Allegretti JR, Yamamoto M, Zhang YZ, Katayama K, Tremmel G, Kawaguchi Y, Shimohigoshi M, Hayashi T, Uematsu M, Yamaguchi K, Furukawa Y, Akiyama Y, Yamaguchi R, Crowe SE, Ernst PB, Miyano S, Kiyono H, Imoto S, and Uematsu S
- Subjects
- Adult, Aged, Bacteriophages, Clostridioides difficile, Enterocolitis, Pseudomembranous microbiology, Feces microbiology, Female, Gastrointestinal Tract virology, Humans, Male, Metagenomics, Microviridae, Middle Aged, Proteobacteria, Enterocolitis, Pseudomembranous therapy, Fecal Microbiota Transplantation, Gastrointestinal Microbiome genetics, Gastrointestinal Tract microbiology, Virome genetics
- Abstract
Background & Aims: Fecal microbiota transplantation (FMT) is an effective therapy for recurrent Clostridioides difficile infection (rCDI). However, the overall mechanisms underlying FMT success await comprehensive elucidation, and the safety of FMT has recently become a serious concern because of the occurrence of drug-resistant bacteremia transmitted by FMT. We investigated whether functional restoration of the bacteriomes and viromes by FMT could be an indicator of successful FMT., Methods: The human intestinal bacteriomes and viromes from 9 patients with rCDI who had undergone successful FMT and their donors were analyzed. Prophage-based and CRISPR spacer-based host bacteria-phage associations in samples from recipients before and after FMT and in donor samples were examined. The gene functions of intestinal microorganisms affected by FMT were evaluated., Results: Metagenomic sequencing of both the viromes and bacteriomes revealed that FMT does change the characteristics of intestinal bacteriomes and viromes in recipients after FMT compared with those before FMT. In particular, many Proteobacteria, the fecal abundance of which was high before FMT, were eliminated, and the proportion of Microviridae increased in recipients. Most temperate phages also behaved in parallel with the host bacteria that were altered by FMT. Furthermore, the identification of bacterial and viral gene functions before and after FMT revealed that some distinctive pathways, including fluorobenzoate degradation and secondary bile acid biosynthesis, were significantly represented., Conclusions: The coordinated action of phages and their host bacteria restored the recipients' intestinal flora. These findings show that the restoration of intestinal microflora functions reflects the success of FMT., (Copyright © 2021 AGA Institute. Published by Elsevier Inc. All rights reserved.)
- Published
- 2021
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10. Metagenome Data on Intestinal Phage-Bacteria Associations Aids the Development of Phage Therapy against Pathobionts.
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Fujimoto K, Kimura Y, Shimohigoshi M, Satoh T, Sato S, Tremmel G, Uematsu M, Kawaguchi Y, Usui Y, Nakano Y, Hayashi T, Kashima K, Yuki Y, Yamaguchi K, Furukawa Y, Kakuta M, Akiyama Y, Yamaguchi R, Crowe SE, Ernst PB, Miyano S, Kiyono H, Imoto S, and Uematsu S
- Subjects
- Animals, Anti-Bacterial Agents pharmacology, Bacteriophages isolation & purification, Clostridium Infections therapy, Disease Models, Animal, Endopeptidases pharmacology, Feces microbiology, Female, Genome, Bacterial, Genome, Viral, Humans, Metagenome, Mice, Mice, Inbred C57BL, Sequence Analysis, DNA, Specific Pathogen-Free Organisms, Viral Proteins genetics, Viral Proteins pharmacology, Bacteriophages genetics, Clostridioides difficile virology, Endopeptidases genetics, Gastrointestinal Microbiome genetics, Phage Therapy methods, Prophages genetics
- Abstract
The application of bacteriophages (phages) is proposed as a highly specific therapy for intestinal pathobiont elimination. However, the infectious associations between phages and bacteria in the human intestine, which is essential information for the development of phage therapies, have yet to be fully elucidated. Here, we report the intestinal viral microbiomes (viromes), together with bacterial microbiomes (bacteriomes), in 101 healthy Japanese individuals. Based on the genomic sequences of bacteriomes and viromes from the same fecal samples, the host bacteria-phage associations are illustrated for both temperate and virulent phages. To verify the usefulness of the comprehensive host bacteria-phage information, we screened Clostridioides difficile-specific phages and identified antibacterial enzymes whose activity is confirmed both in vitro and in vivo. These comprehensive metagenome analyses reveal not only host bacteria-phage associations in the human intestine but also provide vital information for the development of phage therapies against intestinal pathobionts., Competing Interests: Declaration of Interests The authors declare no competing interests., (Copyright © 2020 Elsevier Inc. All rights reserved.)
- Published
- 2020
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11. Antigen-Specific Mucosal Immunity Regulates Development of Intestinal Bacteria-Mediated Diseases.
- Author
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Fujimoto K, Kawaguchi Y, Shimohigoshi M, Gotoh Y, Nakano Y, Usui Y, Hayashi T, Kimura Y, Uematsu M, Yamamoto T, Akeda Y, Rhee JH, Yuki Y, Ishii KJ, Crowe SE, Ernst PB, Kiyono H, and Uematsu S
- Subjects
- Adjuvants, Immunologic administration & dosage, Animals, Bacterial Proteins immunology, Cholera Toxin immunology, Diarrhea diagnosis, Diarrhea immunology, Diarrhea microbiology, Disease Models, Animal, Dysbiosis microbiology, Female, Germ-Free Life, Humans, Intestinal Mucosa microbiology, Male, Mice, Pneumonia diagnosis, Pneumonia immunology, Pneumonia microbiology, Severity of Illness Index, Dysbiosis immunology, Gastrointestinal Microbiome immunology, Immunity, Mucosal, Intestinal Mucosa immunology
- Abstract
Background & Aims: Dysregulation of the microbiome has been associated with development of complex diseases, such as obesity and diabetes. However, no method has been developed to control disease-associated commensal microbes. We investigated whether immunization with microbial antigens, using CpG oligodeoxynucleotides and/or curdlan as adjuvants, induces systemic antigen-specific IgA and IgG production and affects development of diseases in mice., Methods: C57BL/6 mice were given intramuscular injections of antigens (ovalbumin, cholera toxin B-subunit, or pneumococcal surface protein A) combined with CpG oligodeoxynucleotides and/or curdlan. Blood and fecal samples were collected weekly and antigen-specific IgG and IgA titers were measured. Lymph nodes and spleens were collected and analyzed by enzyme-linked immunosorbent assay for antigen-specific splenic T-helper 1 cells, T-helper 17 cells, and memory B cells. Six weeks after primary immunization, mice were given a oral, nasal, or vaginal boost of ovalbumin; intestinal lamina propria, bronchial lavage, and vaginal swab samples were collected and antibodies and cytokines were measured. Some mice were also given oral cholera toxin or intranasal Streptococcus pneumoniae and the severity of diarrhea or pneumonia was analyzed. Gnotobiotic mice were gavaged with fecal material from obese individuals, which had a high abundance of Clostridium ramosum (a commensal microbe associated with obesity and diabetes), and were placed on a high-fat diet 2 weeks after immunization with C ramosum. Intestinal tissues were collected and analyzed by quantitative real-time polymerase chain reaction., Results: Serum and fecal samples from mice given injections of antigens in combination with CpG oligodeoxynucleotides and curdlan for 3 weeks contained antigen-specific IgA and IgG, and splenocytes produced interferon-gamma and interleukin 17A. Lamina propria, bronchial, and vaginal samples contained antigen-specific IgA after the ovalbumin boost. This immunization regimen prevented development of diarrhea after injection of cholera toxin, and inhibited lung colonization by S pneumoniae. In gnotobiotic mice colonized with C ramosum and placed on a high-fat diet, the mice that had been immunized with C ramosum became less obese than the nonimmunized mice., Conclusions: Injection of mice with microbial antigens and adjuvant induces antigen-specific mucosal and systemic immune responses. Immunization with S pneumoniae antigen prevented lung infection by this bacteria, and immunization with C ramosum reduced obesity in mice colonized with this microbe and placed on a high-fat diet. This immunization approach might be used to protect against microbe-associated disorders of intestine., (Copyright © 2019 AGA Institute. Published by Elsevier Inc. All rights reserved.)
- Published
- 2019
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12. A new subset of CD103+CD8alpha+ dendritic cells in the small intestine expresses TLR3, TLR7, and TLR9 and induces Th1 response and CTL activity.
- Author
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Fujimoto K, Karuppuchamy T, Takemura N, Shimohigoshi M, Machida T, Haseda Y, Aoshi T, Ishii KJ, Akira S, and Uematsu S
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- Animals, Antigens, CD immunology, Antigens, CD metabolism, CD8 Antigens immunology, CD8 Antigens metabolism, CD8-Positive T-Lymphocytes immunology, CD8-Positive T-Lymphocytes metabolism, Cell Proliferation, Cells, Cultured, Cytotoxicity, Immunologic immunology, Dendritic Cells metabolism, Flow Cytometry, Forkhead Transcription Factors immunology, Forkhead Transcription Factors metabolism, Integrin alpha Chains immunology, Integrin alpha Chains metabolism, Interleukin-12 Subunit p40 immunology, Interleukin-12 Subunit p40 metabolism, Interleukin-6 immunology, Interleukin-6 metabolism, Intestinal Mucosa immunology, Intestinal Mucosa metabolism, Intestine, Small metabolism, Mice, Mice, Inbred C57BL, Mice, Transgenic, Reverse Transcriptase Polymerase Chain Reaction, T-Lymphocytes, Cytotoxic metabolism, T-Lymphocytes, Regulatory immunology, T-Lymphocytes, Regulatory metabolism, Th1 Cells metabolism, Toll-Like Receptor 3 genetics, Toll-Like Receptor 3 immunology, Toll-Like Receptor 3 metabolism, Toll-Like Receptor 7 genetics, Toll-Like Receptor 7 immunology, Toll-Like Receptor 7 metabolism, Toll-Like Receptor 9 genetics, Toll-Like Receptor 9 immunology, Toll-Like Receptor 9 metabolism, Toll-Like Receptors genetics, Toll-Like Receptors metabolism, Dendritic Cells immunology, Intestine, Small immunology, T-Lymphocytes, Cytotoxic immunology, Th1 Cells immunology, Toll-Like Receptors immunology
- Abstract
CD103(+) dendritic cells (DCs) are the major conventional DC population in the intestinal lamina propria (LP). Our previous report showed that a small number of cells in the LP could be classified into four subsets based on the difference in CD11c/CD11b expression patterns: CD11c(hi)CD11b(lo) DCs, CD11c(hi)CD11b(hi) DCs, CD11c(int)CD11b(int) macrophages, and CD11c(int)CD11b(hi) eosinophils. The CD11c(hi)CD11b(hi) DCs, which are CD103(+), specifically express TLR5 and induce the differentiation of naive B cells into IgA(+) plasma cells. These DCs also mediate the differentiation of Ag-specific Th17 and Th1 cells in response to flagellin. We found that small intestine CD103(+) DCs of the LP (LPDCs) could be divided into a small subset of CD8α(+) cells and a larger subset of CD8α(-) cells. Flow cytometry analysis revealed that CD103(+)CD8α(+) and CD103(+)CD8α(-) LPDCs were equivalent to CD11c(hi)CD11b(lo) and CD11c(hi)CD11b(hi) subsets, respectively. We analyzed a novel subset of CD8α(+) LPDCs to elucidate their immunological function. CD103(+)CD8α(+) LPDCs expressed TLR3, TLR7, and TLR9 and produced IL-6 and IL-12p40, but not TNF-α, IL-10, or IL-23, following TLR ligand stimulation. CD103(+)CD8α(+) LPDCs did not express the gene encoding retinoic acid-converting enzyme Raldh2 and were not involved in T cell-independent IgA synthesis or Foxp3(+) regulatory T cell induction. Furthermore, CD103(+)CD8α(+) LPDCs induced Ag-specific IgG in serum, a Th1 response, and CTL activity in vivo. Accordingly, CD103(+)CD8α(+) LPDCs exhibit a different function from CD103(+)CD8α(-) LPDCs in active immunity. This is the first analysis, to our knowledge, of CD8α(+) DCs in the LP of the small intestine.
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- 2011
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