Researchers

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SUGISAWA Ryoichi: Research associate

Faculty	Department of Medicine
Researchmap	https://researchmap.jp/r_sugisawa

Education and Career

Education

2007/04 - 2013/03 , Nippon Veterinary and Life science University, Faculty of Veterinary Science,
2013/04 - 2017/03 , The University of Tokyo, Faculty of Medicine,

Academic & Professional Experience

Apr. 2023 - Today , Kindai University, Faculty of Medicine Dept. of Biochemistry Assistant Professor
Dec. 2017 - Mar. 2023 , Trinity College Dublin School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute Research Fellow
Apr. 2017 - Nov. 2017 , The University of Tokyo, Faculty of Medicine Project Assistant Professor

Research Activities

Research Areas

Life sciences, Pathobiochemistry
Life sciences, Immunology
Life sciences, Medical biochemistry
Life sciences, Veterinary medicine

Research Interests

Macrophage, Innate Immunity, Inflammation, Immunometabolism, TLR, Inflammasome, NADase, Auto immune disease, Fatty liver, Obesity, Kidney disease, Neuronal disorder, Axon degeneration, Transgenic mice models, Cat / Felis catus, AIM / CD5L, SARM1, NAD

Published Papers

SARM1 regulates pro-inflammatory cytokine expression in human monocytes by NADase-dependent and -independent mechanisms
Ryoichi Sugisawa; Katharine A. Shanahan; Gavin Davis; Gavin Davey; Andrew G. Bowie
iScience , 109940-109940, May. 2024 , Refereed
Deoxycytidine kinase inactivation enhances gemcitabine resistance and sensitizes mitochondrial metabolism interference in pancreatic cancer
Suman Dash; Takeshi Ueda; Akiyoshi Komuro; Masahiko Honda; Ryoichi Sugisawa; Hitoshi Okada
Cell Death & Disease 12, Feb. 2024 , Refereed
SARM1 regulates NAD+-linked metabolism and select immune genes in macrophages
Katharine A. Shanahan; Gavin M. Davis; Ciara G. Doran; Ryoichi Sugisawa; Gavin P. Davey; Andrew G. Bowie
Journal of Biological Chemistry Jan. 2024 , Refereed

SARM1 regulates pro-inflammatory cytokine expression in human monocytes by NADase-dependent and -independent mechanisms , Ryoichi Sugisawa; Andrew Bowie , The 46th Annual Meeting of the Molecular Biology Society of Japan , 8, Dec. 2023
SARM1 regulates pro-inflammatory cytokine expression by NADase-dependent and -independent mechanism , Ryoichi Sugisawa; Andrew Bowie , The 166th meeting of the Japanese Society of Veterinary Science , Sep. 2023
SARM1 regulates pro-inflammatory cytokine expression in human monocytes by NADase-dependent and -independent mechanisms , Ryoichi Sugisawa; Andrew G Bowie , Irish Society for Immunology Annual Meeting 2022 , 1, Sep. 2022

Klebsiella pneumoniae hijacks the Toll-IL-1R protein SARM1 in a type I IFN-dependent manner to antagonize host immunity , Claudia Feriotti; Joana Sa-Pessoa; Ricardo Calderón-González; Lili Gu; Brenda Morris; Ryoichi Sugisawa; Jose L. Insua; Michael Carty; Amy Dumigan; Rebecca J. Ingram; Adrien Kisenpfening; Andrew G. Bowie; José A. Bengoechea , bioRxiv , 29, Sep. 2021
Summary:<title>SUMMARY</title>Many bacterial pathogens antagonize host defence responses by translocating effector proteins into cells. It remains an open question how those pathogens not encoding effectors counteract anti-bacterial immunity. Here, we show that <italic>Klebsiella pneumoniae</italic> hijacks the evolutionary conserved innate immune protein SARM1 to control cell intrinsic immunity. <italic>Klebsiella</italic> exploits SARM1 to regulate negatively MyD88 and TRIF-governed inflammation, and the activation of the MAP kinases ERK and JNK. SARM1 is required for <italic>Klebsiella</italic> induction of IL10 by fine-tuning the p38-type I IFN axis. SARM1 inhibits the activation of <italic>Klebsiella</italic>-induced absent in melanoma 2 inflammasome to limit IL1β production, suppressing further inflammation. <italic>Klebsiella</italic> exploits type I IFNs to induce SARM1 in a capsule and LPS O-polysaccharide-dependent manner via TLR4-TRAM-TRIF-IRF3-IFNAR1 pathway. Absence of SARM1 reduces the intracellular survival of <italic>K. pneumonaie</italic> in macrophages whereas <italic>sarm1</italic> deficient mice control the infection. Altogether, our results illustrate a hitherto unknown anti-immunology strategy deployed by a human pathogen.
Next generation SARM1 knockout and epitope tagged CRISPR-Cas9-generated isogenic mice reveal that SARM1 does not participate in regulating nuclear transcription, despite confirmation of protein expression in macrophages , Ciara G. Doran; Ryoichi Sugisawa; Michael Carty; Fiona Roche; Claire Fergus; Karsten Hokamp; Vincent P. Kelly; Andrew G Bowie , bioRxiv , 25, Aug. 2021
Summary:<title>ABSTRACT</title>SARM1 is an ancient and highly conserved TIR-domain containing protein, with a diverse range of proposed roles in both innate immunity and neuronal death and degeneration. Murine SARM1 has been reported to regulate the transcription of specific chemokines in both neurons and macrophages, however the extent and mechanism by which SARM1 contributes to transcription regulation remains to be fully understood. Here, using RNA sequencing we identify differential gene expression in bone marrow-derived macrophages (BMDM) from C57BL/6 congenic 129 ES cell-derived <italic>Sarm1</italic><sup>-/-</sup> mice compared to wild type (WT). However, we show that passenger genes which are derived from the 129 donor strain of mice flank the <italic>Sarm1</italic> locus, confounding interpretation of results, since many of the identified differentially regulated genes come from the region containing passenger genes. To re-examine the transcriptional role of SARM1 in the absence of such passenger genes, we generated three different <italic>Sarm1</italic><sup>-/-</sup> mice using CRISPR/Cas9 technology. Vincristine treatment of <italic>ex vivo</italic> cultured post-natal neurons from these mice confirmed SARM1’s previously identified key function as an executor of axon degeneration. However, using these mice, we show that the absence of SARM1 has no impact on transcription of genes previously shown to be altered in macrophages or in the brainstem. To gain further insight into SARM1 function, we generated and characterized a mouse expressing epitope-tagged SARM1, as it has been difficult to date to confirm which cells and tissues express SARM1 protein. In these mice we see high SARM1 protein expression in the brain and brainstem, and lower but detectable levels in macrophages. Overall, the generation of these next generation SARM1 knockout and epitope-tagged mice has clarified that SARM1 is expressed in mouse macrophages but has no general role in transcriptional regulation in these cells, and has provided important new animal models to further explore SARM1 function.
Generation and initial characterization of a SARM epitope-tagged mouse , Ryoichi Sugisawa; Ciara G Doran; Andrew G Bowie , European Journal of Immunology , 51 , (Suppl. 1) , 207 , 207 , Aug. 2021

Sep. 2021, EFIS (European Federation of Immunological Societies), Waived Registration Grant (for Virtual 6th European Congress of Immunology - ECI 2021)
Sep. 2019, The Japanese Society of Veterinary Science, Veterinary Science Young Investigator Awards
Nov. 2018, HOST-PATHOGEN COMMUNICATION, TRAVEL AWARD

Japan Society for the Promotion of Science(JSPS), KAKENHI, Elucidating the role of SARM1 in senescence and aging related diseases , Kinki University
Kindai University, Kindai University Research Enchancement Grant, 2023 Kindai University Research Enchancement Grant , Kinki University
Japan Society for the Promotion of Science(JSPS), KAKENHI, Elucidating the role of SARM1 under inflammation , Kinki University