Updated on 2024/01/04

写真a

 
ITO Ayaka
 
Organization
Research Institute of Environmental Medicine Division of Stress Recognition and Response Lecturer
Graduate School
Graduate School of Medicine
Title
Lecturer
Contact information
メールアドレス

Degree 3

  1. Ph.D. (Medical Science) ( 2008.3   Tokyo Medical and Dental University ) 

  2. 修士(農学) ( 2004.3   京都大学 ) 

  3. 学士(生活環境学) ( 2002.3   奈良女子大学 ) 

Research Interests 8

  1. immunometabolism

  2. nuclear receptor

  3. lipid metabolism

  4. Autoimmune disease

  5. Immunology

  6. 心身相関

  7. Immunometabolism

  8. Lipid metabolism

Research Areas 3

  1. Life Science / Pathological biochemistry

  2. Life Science / Nutrition science and health science  / 栄養学および健康科学

  3. Life Science / Metabolism and endocrinology

Current Research Project and SDGs 1

  1. 慢性炎症性疾患における脂質代謝の意義の解明

Research History 8

  1. Nagoya University   Lecturer

    2021.11

  2. Nagoya University   Lecturer

    2021.11

  3. 名古屋大学 高等研究院   若手新分野創成研究ユニット 心身相関病態研究ユニット   講師(兼務)

    2021.11

  4. 名古屋大学 環境医学研究所   分子代謝医学分野   講師

    2021.11

  5. 名古屋大学 高等研究院   若手新分野創成研究ユニット 心身相関病態研究ユニット   助教(兼務)

    2020.4 - 2021.10

  6. Nagoya University   Research Institute of Environmental Medicine   Assistant Professor

    2018.4 - 2021.10

  7. Nagoya University   Research Institute of Environmental Medicine   Adjunct Assistant Professor

    2017.6 - 2018.3

  8. Nagoya University   Research Institute of Environmental Medicine   Researcher

    2016.9 - 2017.5

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Education 3

  1. Tokyo Medical and Dental University

    2004.4 - 2008.3

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    Country: Japan

  2. Kyoto University

    2002.4 - 2004.3

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    Country: Japan

  3. Nara Women's University   Faculty of Living Environmental Studies

    1998.4 - 2002.3

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    Country: Japan

Professional Memberships 6

  1. JAPAN SOCIETY FOR THE STUDY OF OBESITY

  2. JAPAN SOCIETY OF NUTRITION AND FOOD SCIENCE

  3. The Japan Endocrine Society

  4. THE JAPANESE SOCIETY FOR IMMUNOLOGY

  5. 日本脂質生化学会

  6. 日本生化学会

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Committee Memberships 1

  1. 日本内分泌学会   評議員  

    2020.4 - 2024.3   

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    Committee type:Academic society

Awards 3

  1. Young Investigator Award

    2018.4   Japan Society of Molecular Medicine  

    Ayaka Ito

  2. 若手研究奨励賞

    2014   日本内分泌学会  

  3. 若手研究奨励賞

    2007   日本肥満学会  

 

Papers 23

  1. Lysosomal cholesterol overload in macrophages promotes liver fibrosis in a mouse model of NASH. International journal

    Michiko Itoh, Atsushi Tamura, Sayaka Kanai, Miyako Tanaka, Yohei Kanamori, Ibuki Shirakawa, Ayaka Ito, Yasuyoshi Oka, Isao Hidaka, Taro Takami, Yasushi Honda, Mitsuyo Maeda, Yasuyuki Saito, Yoji Murata, Takashi Matozaki, Atsushi Nakajima, Yosky Kataoka, Tomoo Ogi, Yoshihiro Ogawa, Takayoshi Suganami

    The Journal of experimental medicine   Vol. 220 ( 11 )   2023.9

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    Accumulation of lipotoxic lipids, such as free cholesterol, induces hepatocyte death and subsequent inflammation and fibrosis in the pathogenesis of nonalcoholic steatohepatitis (NASH). However, the underlying mechanisms remain unclear. We have previously reported that hepatocyte death locally induces phenotypic changes in the macrophages surrounding the corpse and remnant lipids, thereby promoting liver fibrosis in a murine model of NASH. Here, we demonstrated that lysosomal cholesterol overload triggers lysosomal dysfunction and profibrotic activation of macrophages during the development of NASH. β-cyclodextrin polyrotaxane (βCD-PRX), a unique supramolecule, is designed to elicit free cholesterol from lysosomes. Treatment with βCD-PRX ameliorated cholesterol accumulation and profibrotic activation of macrophages surrounding dead hepatocytes with cholesterol crystals, thereby suppressing liver fibrosis in a NASH model, without affecting the hepatic cholesterol levels. In vitro experiments revealed that cholesterol-induced lysosomal stress triggered profibrotic activation in macrophages predisposed to the steatotic microenvironment. This study provides evidence that dysregulated cholesterol metabolism in macrophages would be a novel mechanism of NASH.

    DOI: 10.1084/jem.20220681

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  2. Novel Therapeutic Potentials of Taxifolin for Obesity-Induced Hepatic Steatosis, Fibrogenesis, and Tumorigenesis Invited Reviewed International journal

    Takayuki Inoue, Bin Fu, Miwako Nishio, Miyako Tanaka, Hisashi Kato, Masashi Tanaka, Michiko Itoh, Hajime Yamakage, Kozue Ochi, Ayaka Ito, Yukihiro Shiraki, Satoshi Saito, Masafumi Ihara, Hideo Nishimura, Atsuhiko Kawamoto, Shian Inoue, Kumiko Saeki, Atsushi Enomoto, Takayoshi Suganami, Noriko Satoh-Asahara

    Nutrients   Vol. 15 ( 2 ) page: 350   2023.1

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    The molecular pathogenesis of nonalcoholic steatohepatitis (NASH) includes a complex interaction of metabolic stress and inflammatory stimuli. Considering the therapeutic goals of NASH, it is important to determine whether the treatment can prevent the progression from NASH to hepatocellular carcinoma. Taxifolin, also known as dihydroquercetin, is a natural bioactive flavonoid with antioxidant and anti-inflammatory properties commonly found in various foods and health supplement products. In this study, we demonstrated that Taxifolin treatment markedly prevented the development of hepatic steatosis, chronic inflammation, and liver fibrosis in a murine model of NASH. Its mechanisms include a direct action on hepatocytes to inhibit lipid accumulation. Taxifolin also increased brown adipose tissue activity and suppressed body weight gain through at least two distinct pathways: direct action on brown adipocytes and indirect action via fibroblast growth factor 21 production in the liver. Notably, the Taxifolin treatment after NASH development could effectively prevent the development of liver tumors. Collectively, this study provides evidence that Taxifolin shows pleiotropic effects for the treatment of the NASH continuum. Our data also provide insight into the novel mechanisms of action of Taxifolin, which has been widely used as a health supplement with high safety.

    DOI: 10.3390/nu15020350

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  3. The sodium-glucose cotransporter-2 inhibitor Tofogliflozin prevents the progression of nonalcoholic steatohepatitis-associated liver tumors in a novel murine model. International journal

    Naoki Yoshioka, Miyako Tanaka, Kozue Ochi, Akiko Watanabe, Kenji Ono, Makoto Sawada, Tomoo Ogi, Michiko Itoh, Ayaka Ito, Yukihiro Shiraki, Atsushi Enomoto, Masatoshi Ishigami, Mitsuhiro Fujishiro, Yoshihiro Ogawa, Takayoshi Suganami

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie   Vol. 140   page: 111738 - 111738   2021.8

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    BACKGROUND: Diabetes and obesity contribute to the pathogenesis of nonalcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC). However, how diabetes and obesity accelerate liver tumorigenesis remains to be fully understood. Moreover, to verify the therapeutic potential of anti-diabetic drugs, there exists a strong need for appropriate animal models that recapitulate human pathophysiology of NASH and HCC. METHODS: We established a novel murine model of NASH-associated liver tumors using genetically obese melanocortin 4 receptor-deficient mice fed on Western diet in combination with a chemical procarcinogen, and verified the validity of our model in evaluating drug efficacy. FINDINGS: Our model developed multiple liver tumors together with obesity, diabetes, and NASH within a relatively short period (approximately 3 months). In this model, sodium glucose cotransporter 2 inhibitor Tofogliflozin prevented the development of NASH-like liver phenotypes and the progression of liver tumors. Tofogliflozin attenuated p21 expression of hepatocytes in non-tumorous lesions in the liver. INTERPRETATION: Tofogliflozin treatment attenuates cellular senescence of hepatocytes under obese and diabetic conditions. This study provides a unique animal model of NASH-associated liver tumors, which is applicable for assessing drug efficacy to prevent or treat NASH-associated HCC.

    DOI: 10.1016/j.biopha.2021.111738

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  4. Dietary Supplementation With Eicosapentaenoic Acid Inhibits Plasma Cell Differentiation and Attenuates Lupus Autoimmunity

    Azusa Kobayashi, Ayaka Ito, Ibuki Shirakawa, Atsushi Tamura, Susumu Tomono, Hideo Shindou, Per Niklas Hedde, Miyako Tanaka, Naotake Tsuboi, Takuji Ishimoto, Sachiko Akashi-Takamura, Shoichi Maruyama, Takayoshi Suganami

    Frontiers in Immunology   Vol. 12   page: 650856   2021.6

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Frontiers Media SA  

    Accumulating evidence suggests that cholesterol accumulation in leukocytes is causally associated with the development of autoimmune diseases. However, the mechanism by which fatty acid composition influences autoimmune responses remains unclear. To determine whether the fatty acid composition of diet modulates leukocyte function and the development of systemic lupus erythematosus, we examined the effect of eicosapentaenoic acid (EPA) on the pathology of lupus in drug-induced and spontaneous mouse models. We found that dietary EPA supplementation ameliorated representative lupus manifestations, including autoantibody production and immunocomplex deposition in the kidneys. A combination of lipidomic and membrane dynamics analyses revealed that EPA remodels the lipid composition and fluidity of B cell membranes, thereby preventing B cell differentiation into autoantibody-producing plasma cells. These results highlight a previously unrecognized mechanism by which fatty acid composition affects B cell differentiation into autoantibody-producing plasma cells during autoimmunity, and imply that EPA supplementation may be beneficial for therapy of lupus.

    DOI: 10.3389/fimmu.2021.650856

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  5. Macrophages rely on extracellular serine to suppress aberrant cytokine production. International journal

    Kento Kurita, Hiroya Ohta, Ibuki Shirakawa, Miyako Tanaka, Yasuyuki Kitaura, Yorihiro Iwasaki, Takashi Matsuzaka, Hitoshi Shimano, Seiichiro Aoe, Hiroshi Arima, Yoshihiro Ogawa, Ayaka Ito, Takayoshi Suganami

    Scientific reports   Vol. 11 ( 1 ) page: 11137 - 11137   2021.5

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    A growing body of evidence indicates that cellular metabolism is involved in immune cell functions, including cytokine production. Serine is a nutritionally non-essential amino acid that can be generated by de novo synthesis and conversion from glycine. Serine contributes to various cellular responses, but the role in inflammatory responses remains poorly understood. Here, we show that macrophages rely on extracellular serine to suppress aberrant cytokine production. Depleting serine from the culture media reduced the cellular serine content in macrophages markedly, suggesting that macrophages depend largely on extracellular serine rather than cellular synthesis. Under serine deprivation, macrophages stimulated with lipopolysaccharide showed aberrant cytokine expression patterns, including a marked reduction of anti-inflammatory interleukin-10 expression and sustained expression of interleukine-6. Transcriptomic and metabolomics analyses revealed that serine deprivation causes mitochondrial dysfunction: reduction in the pyruvate content, the NADH/NAD+ ratio, the oxygen consumption rate, and the mitochondrial production of reactive oxygen species (ROS). We also found the role of mitochondrial ROS in appropriate cytokine production. Thus, our results indicate that cytokine production in macrophages is tightly regulated by the nutritional microenvironment.

    DOI: 10.1038/s41598-021-90086-w

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  6. NASHにおけるクッパー細胞鉄代謝の病態生理学的意義

    金森 耀平, 田中 都, 伊藤 美智子, 越智 梢, 伊藤 綾香, 日高 勲, 坂井田 功, 小川 佳宏, 菅波 孝祥

    日本内分泌学会雑誌   Vol. 97 ( 1 ) page: 255 - 255   2021.4

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    Language:Japanese   Publisher:(一社)日本内分泌学会  

  7. Iron-rich Kupffer cells exhibit phenotypic changes during the development of liver fibrosis in NASH. International journal

    Yohei Kanamori, Miyako Tanaka, Michiko Itoh, Kozue Ochi, Ayaka Ito, Isao Hidaka, Isao Sakaida, Yoshihiro Ogawa, Takayoshi Suganami

    iScience   Vol. 24 ( 2 ) page: 102032 - 102032   2021.2

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    Although recent evidence suggests the involvement of iron accumulation in the pathogenesis of nonalcoholic steatohepatitis (NASH), the underlying mechanisms remain poorly understood. Previously, we reported a unique histological structure termed "crown-like structure (CLS)," where liver-resident macrophages (Kupffer cells) surround dead hepatocytes, scavenge their debris, and induce inflammation and fibrosis in NASH. In this study, using magnetic column separation, we show that iron-rich Kupffer cells exhibit proinflammatory and profibrotic phenotypic changes during the development of NASH, at least partly, through activation of MiT/TFE transcription factors. Activation of MiT/TFE transcription factors is observed in Kupffer cells forming CLSs in murine and human NASH. Iron chelation effectively attenuates liver fibrosis in a murine NASH model. This study provides insight into the pathophysiologic role of iron in NASH. Our data also shed light on a unique macrophage subset rich in iron that contributes to CLS formation and serves as a driver of liver fibrosis.

    DOI: 10.1016/j.isci.2020.102032

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  8. C-type lectin Mincle mediates cell death-triggered inflammation in acute kidney injury. Reviewed International journal

    Miyako Tanaka, Marie Saka-Tanaka, Kozue Ochi, Kumiko Fujieda, Yuki Sugiura, Tomofumi Miyamoto, Hiro Kohda, Ayaka Ito, Taiki Miyazawa, Akira Matsumoto, Seiichiro Aoe, Yoshihiro Miyamoto, Naotake Tsuboi, Shoichi Maruyama, Makoto Suematsu, Sho Yamasaki, Yoshihiro Ogawa, Takayoshi Suganami

    The Journal of experimental medicine   Vol. 217 ( 11 )   2020.11

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    Accumulating evidence indicates that cell death triggers sterile inflammation and that impaired clearance of dead cells causes nonresolving inflammation; however, the underlying mechanisms are still unclear. Here, we show that macrophage-inducible C-type lectin (Mincle) senses renal tubular cell death to induce sustained inflammation after acute kidney injury in mice. Mincle-deficient mice were protected against tissue damage and subsequent atrophy of the kidney after ischemia-reperfusion injury. Using lipophilic extract from the injured kidney, we identified β-glucosylceramide as an endogenous Mincle ligand. Notably, free cholesterol markedly enhanced the agonistic effect of β-glucosylceramide on Mincle. Moreover, β-glucosylceramide and free cholesterol accumulated in dead renal tubules in proximity to Mincle-expressing macrophages, where Mincle was supposed to inhibit clearance of dead cells and increase proinflammatory cytokine production. This study demonstrates that β-glucosylceramide in combination with free cholesterol acts on Mincle as an endogenous ligand to induce cell death-triggered, sustained inflammation after acute kidney injury.

    DOI: 10.1084/jem.20192230

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  9. アルツハイマー病モデルにおける神経炎症に対する全身炎症が与える影響の検討

    下川 梨津子, 小峯 起, 伊藤 綾香, 祖父江 顕, 斉藤 貴志, 西道 隆臣, 菅波 孝祥, 山中 宏二

    Dementia Japan   Vol. 34 ( 4 ) page: 528 - 528   2020.10

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    Language:Japanese   Publisher:(一社)日本認知症学会  

  10. Dipeptidyl peptidase-4 inhibition prevents nonalcoholic steatohepatitis-associated liver fibrosis and tumor development in mice independently of its anti-diabetic effects. Reviewed International journal

    Mitsuhiro Kawakubo, Miyako Tanaka, Kozue Ochi, Akiko Watanabe, Marie Saka-Tanaka, Yohei Kanamori, Naoki Yoshioka, Satoko Yamashita, Moritaka Goto, Michiko Itoh, Ibuki Shirakawa, Sayaka Kanai, Hiromi Suzuki, Makoto Sawada, Ayaka Ito, Masatoshi Ishigami, Mitsuhiro Fujishiro, Hiroshi Arima, Yoshihiro Ogawa, Takayoshi Suganami

    Scientific reports   Vol. 10 ( 1 ) page: 983 - 983   2020.1

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    Nonalcoholic steatohepatitis (NASH) is a hepatic phenotype of the metabolic syndrome, and increases the risk of cirrhosis and hepatocellular carcinoma (HCC). Although increasing evidence points to the therapeutic implications of certain types of anti-diabetic agents in NASH, it remains to be elucidated whether their effects on NASH are independent of their effects on diabetes. Genetically obese melanocortin 4 receptor-deficient (MC4R-KO) mice fed Western diet are a murine model that sequentially develops hepatic steatosis, NASH, and HCC in the presence of obesity and insulin resistance. In this study, we investigated the effect of the dipeptidyl peptidase-4 (DPP-4) inhibitor anagliptin on NASH and HCC development in MC4R-KO mice. Anagliptin treatment effectively prevented inflammation, fibrosis, and carcinogenesis in the liver of MC4R-KO mice. Interestingly, anagliptin only marginally affected body weight, systemic glucose and lipid metabolism, and hepatic steatosis. Histological data and gene expression analysis suggest that anagliptin treatment targets macrophage activation in the liver during the progression from simple steatosis to NASH. As a molecular mechanism underlying anagliptin action, we showed that glucagon-like peptide-1 suppressed proinflammatory and profibrotic phenotypes of macrophages in vitro. This study highlights the glucose metabolism-independent effects of anagliptin on NASH and HCC development.

    DOI: 10.1038/s41598-020-57935-6

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  11. Transcriptional regulation of macrophage cholesterol efflux and atherogenesis by a long noncoding RNA.

    Sallam T, Jones M, Thomas BJ, Wu X, Gilliland T, Qian K, Eskin A, Casero D, Zhang Z, Sandhu J, Salisbury D, Rajbhandari P, Civelek M, Hong C, Ito A, Liu X, Daniel B, Lusis AJ, Whitelegge J, Nagy L, Castrillo A, Smale S, Tontonoz P

    Nature medicine   Vol. 24 ( 3 ) page: 304-312   2018.3

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    DOI: 10.1038/nm.4479

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  12. Transcriptional regulation of macrophage cholesterol efflux and atherogenesis by a long noncoding RNA Reviewed

    Sallam T, Jones M, Thomas BJ, Wu X, Gilliland T, Qian K, Eskin A, Casero D, Zhang Z, Sandhu J, Salisbury D, Rajbhandari P, Civelek M, Hong C, Ito A, Liu X, Daniel B, Lusis AJ, Whitelegge J, Nagy L, Castrillo A, Smale S, Tontonoz P

    Nature Medicine   Vol. 24   page: 304 - 312   2018

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  13. Cholesterol accumulation in antigen presenting cells is a causal and targetable factor in autoimmune disease Reviewed

    Ito A, Hong C, Oka K, Salazar JV, Diehl C, Witztum JL, Castrillo A, Bensinger SV, Chan L, Tontonoz P.

    Immunity   Vol. 45 ( 6 ) page: 1311 - 1326   2016

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

  14. LXRs link metabolism to inflammation through Abca1-dependent regulation of membrane composition and TLR signaling Reviewed

    Hong C, Rong X, Zhu X, Tarling EJ, Hedde PN, Gratton E, Parks J, Tontonoz P

    eLife   Vol. 4   page: e08009   2015

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  15. The macrophage lipopolysaccharide binging protein gene is an LXR target that promotes macrophage survival and atherosclerosis Reviewed

    Sallam T, Ito A, Rong X, Kim J, van Stijn C, Chamberlain BT, Jung ME, Chao LC, Jones M, Gilliland T, Wu X, Su GL, Tangirala RK, Tontonoz P, Hong C

    Journal of Lipid Research   Vol. 55   page: 1120 - 1130   2014

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  16. LXRs regulate ER stress and inflammation through dynamic modulation of membrane phospholipid composition. Reviewed

    Rong X, Albert CJ, Hong C, Duerr MA, Chamberlain BT, Tarling EJ, Ito A, Gao J, Wang B, Edwards PA, Jung ME, Ford DA, Tontonoz P.

    Cell Metabolism   Vol. 18   page: 685 - 697   2013

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  17. Bone marrow NR4A expression is not a dominant factor in the development of atherosclerosis or macrophage polarization in mice. Reviewed

    Chao L, Soto E, Hong C, Ito A, Pei L, Chawla A, Conneely O, Tangirala RK, Evans RM, Tontonoz P

    Journal of Lipid Research   Vol. 54   page: 806 - 815   2013

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  18. Hormonal modulators of glial ABCA1 and apoE levels. Reviewed

    Fan J, Shimizu Y, Chan J, Wilkinson A, Ito A, Tontonoz P, Dullaghan E, Galea LA, Pfeifer T

    Journal of Lipid Research   Vol. 54   page: 3139 - 3150   2013

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  19. Coordinate regulation of neutrophil homeostasis by liver X receptors in mice Reviewed

    Hong C, Kidani Y, A-Gonzalez N, Phung T, Ito A, Rong X, Ericson K, Mikkola H, Beaven SW, Miller LS, Shao WH, Cohen PL, Castrillo A, Tontonoz P, Bensinger SJ

    Journal of Clinical Investigation   Vol. 122   page: 337 - 347   2012

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  20. Oxidative stress in the ischemic and non-ischemic parts of the rat liver after two-thirds ischemia/reperfusion Reviewed

    Kitamura Y, Washino Y, Koga E, Ito A, Kawagoe M, Nakazaki C, Kiso K, Ichi I, Matsura T, Kojo S

    Bioscience, Biotechnology, and Biochemistry   Vol. 74   page: 979 - 983   2010

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  21. Role of C-C chemokine receptor 2 in bone marrow cells in the recruitment of macrophages into obese adipose tissue Reviewed

    Ito A, Suganami T, Yamauchi A, Degawa-Yamauchi M, Tanaka M , Kouyama R, Nitta N, Yasuda K, Hirata Y, Kuziel WA, Takeya M, Kanegasaki S, Kamei Y, and Ogawa Y

    Journal of Biological Chemistry   Vol. 283   page: 35715 - 35723   2008

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

  22. Role of MAPK phosphatase-1 in the induction of monocyte chemoattractant protein-1 during the course of adipocyte hypertrophy Reviewed

    Ito A, Suganami T, Miyamoto Y, Yoshimasa Y, Takeya M, Kamei Y, and Ogawa Y

    Journal of Biological Chemistry   Vol. 282   page: 25445 - 25452   2007

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  23. FPRL1 receptor agonist peptides prevent etoposide-induced alopecia in neonatal rats Reviewed

    Tsuruki T, Ito A and Yoshikawa M

    Journal of Investigative Dermatology   Vol. 123   page: 242 - 243   2004

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Books 6

  1. 細胞内脂質代謝による免疫代謝と慢性炎症性疾患

    伊藤パディジャ綾香、菅波孝祥( Role: Joint author)

    実験医学増刊. 羊土社  2022.5  ( ISBN:978-4-7581-0402-9

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    Responsible for pages:7   Language:Japanese Book type:Scholarly book

  2. 動脈硬化と自然免疫

    伊藤綾香、菅波孝祥( Role: Joint author)

    炎症と免疫. 先端医学社  2019 

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    Total pages:5   Language:Japanese

  3. 細胞内脂質代謝とイムノメタボリズム

    伊藤綾香、菅波孝祥( Role: Joint author)

    The Lipid. メディカルレビュー社  2019 

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    Total pages:7   Language:Japanese

  4. 慢性炎症性疾患における脂質代謝異常の意義

    伊藤綾香、菅波孝祥( Role: Joint author)

    内分泌・糖尿病・代謝内科. 科学評論社  2019 

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    Total pages:5   Language:Japanese

  5. メタボリックシンドロームとリポクオリティ

    菅波孝祥、田中都、伊藤綾香、小川佳宏( Role: Joint author)

    実験医学. 羊土社  2018 

  6. 慢性炎症性疾患における脂質クオリティ

    伊藤綾香、菅波孝祥( Role: Joint author)

    医学のあゆみ. 医歯薬出版株式会社  2018 

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    Language:Japanese

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MISC 6

  1. 細胞内脂質代謝による免疫代謝と慢性炎症性疾患 Invited

    伊藤パディジャ綾香, 菅波孝祥

    実験医学増刊「栄養・代謝物シグナルと食品機能」   Vol. 40 ( 7 ) page: 219 - 225   2022.5

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    Authorship:Lead author  

  2. 慢性炎症性疾患における脂質代謝異常の意義 Invited

    伊藤綾香, 菅波孝祥

      Vol. 48 ( 6 ) page: 447 - 451   2019.6

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  3. 動脈硬化と自然炎症 Invited

    伊藤綾香, 菅波孝祥

    炎症と免疫   Vol. 27 ( 4 ) page: 70 - 74   2019.6

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  4. 細胞内脂質代謝とイムノメタボリズム Invited

    伊藤綾香, 菅波孝祥

    The Lipid   Vol. 30 ( 2 ) page: 15 - 21   2019.4

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  5. Metabolic syndrome and lipoquality Invited

    Suganami T, Tanaka M, Ito A, Ogawa Y

    Experimental Medicine   Vol. 36 ( 10 ) page: 174 - 179   2018

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    Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media)  

  6. Lipoquality in chronic inflammatory diseases Invited

    Ito A, Suganami T

    Journal of Clinical and Experimental Medicine   Vol. 264 ( 11 ) page: 944 - 948   2018

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    Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media)  

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Presentations 27

  1. Cellular lipid metabolism in systemic lupus erythematosus Invited

    2023.6.11 

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    Event date: 2023.6

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

  2. 慢性炎症性疾患における細胞内脂質代謝の意義の解明 Invited

    伊藤パディジャ綾香

    第96回 日本内分泌学会学術総会  2023.6.2 

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    Event date: 2023.6

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

  3. Molecular crosstalk between lipid metabolism, inflammation and autoimmunity Invited

    2023.3.15 

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    Event date: 2023.3

    Language:English   Presentation type:Symposium, workshop panel (public)  

  4. 中枢ー末梢連関による生体恒常性維持と疾患 Invited

    伊藤パディジャ綾香、片岡直也

    第95回 日本生化学会大会  2022.11.9 

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    Event date: 2022.11

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

  5. 細胞内脂質代謝異常による炎症・自己免疫制御破綻のメカニズム Invited

    伊藤パディジャ綾香

    第95回 日本生化学会大会  2022.11.9 

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    Event date: 2022.11

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

  6. 細胞内脂質代謝による免疫代謝と慢性炎症の分子機構 Invited

    伊藤パディジャ綾香

    日本動脈硬化学会創設50周年記念大会(第54回 日本動脈硬化学会総会・学術集会)  2022.7.24 

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    Event date: 2022.7

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:福岡(久留米シティプラザ)  

  7. 自己免疫疾患における抗体産生と多価不飽和脂肪酸の意義の解明

    伊藤パディジャ綾香、白川伊吹、 小林光子、菅波孝祥

    第65回 日本脂質生化学会  2023.6.9 

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    Event date: 2023.6

    Language:Japanese   Presentation type:Oral presentation (general)  

  8. Significance of fatty acid metabolism in lupus autoimmunity and antibody production

    Ayaka Ito

    2023.6.2 

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    Event date: 2023.6

    Language:English   Presentation type:Oral presentation (general)  

  9. グリアを介した脳ー身体連関と末梢免疫応答制御

    伊藤パディジャ綾香

    文部科学省科研費 学術変革領域研究(A)「グリアデコーディング」第5回領域会議  2023.2.9 

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    Event date: 2023.2

    Language:Japanese   Presentation type:Oral presentation (general)  

  10. 細胞内脂質代謝異常による炎症・自己免疫制御破綻の分子機構 Invited

    伊藤パディジャ綾香

    第15回 心・血管クラスターミニリトリート  2023.1.22 

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    Event date: 2023.1

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:徳島(徳島大学病院)  

  11. 細胞内脂質代謝と免疫応答のクロストーク Invited

    伊藤パディジャ綾香

    第40回 内分泌代謝学サマーセミナー  2022.7.8 

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    Event date: 2022.7

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

  12. 抗体産生における多価不飽和脂肪酸代謝の意義の解明

    伊藤綾香、小林アズサ、白川伊吹、小林光子、菅波孝祥

    第64回 脂質生化学会  2022.6.23 

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    Event date: 2022.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:東京  

  13. 抗体産生における多価不飽和脂肪酸代謝の意義の解明

    伊藤綾香、小林アズサ、白川伊吹、小林光子、菅波孝祥

    第76回 日本栄養食糧学会大会  2022.6.11 

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    Event date: 2022.6

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:兵庫  

  14. 抗体産生による脂肪酸代謝の意義の解明

    伊藤綾香、小林アズサ、白川伊吹、小林光子、菅波孝祥

    第95回日本内分泌学会学術総会  2022.6.2 

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    Event date: 2022.6

    Language:Japanese   Presentation type:Oral presentation (general)  

  15. Dietary supplementation with eicosapentaenoic acid inhibits plasma cell differentiation and attenuates lupus autoimmunity International coauthorship

    Ayaka Ito, Azusa Kobayashi, Ibuki Shirakawa, Atsushi Tamura, Susumu Tomono, Hideo Shindou, Per Niklas Hedde, Miyako Tanaka, Naotake Tsuboi, Takuji Ishimoto, Sachiko Akashi-Takamura, Shoichi Maruyama, Takayoshi Suganami

    2021.12 

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    Event date: 2021.12

    Language:English  

  16. グリア内脂質代謝を介した脳-身体連関と末梢自己免疫応答制御の解明

    伊藤綾香

    文部科学省科研費 学術変革領域研究(A)「グリアデコーディング」第3回領域会議  2021.12 

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    Event date: 2021.12

  17. 全身性自己免疫疾患における免疫細胞内脂肪酸組成の意義の解明

    伊藤綾香, 小林アズサ, 白川伊吹, 伴野勧, 田村篤志, 高村(赤司)祥子, 菅波孝祥

    第75回 日本栄養食糧学会大会  2021.7 

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    Event date: 2021.7

    Language:Japanese  

  18. 全身性エリテマトーデスにおける免疫細胞内脂肪酸組成の意義の解明

    伊藤綾香, 小林アズサ, 白川伊吹, 伴野勧, 田村篤志, 菅波孝祥

    第94回日本内分泌学会学術総会  2021.4 

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    Event date: 2021.4

    Language:Japanese  

  19. 自己免疫応答におけるオメガ3脂肪酸の意義

    伊藤綾香, 小林アズサ, 白川伊吹, 菅波孝祥

    第74回日本栄養・食糧学会大会 

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    Event date: 2020.5

  20. 自己免疫応答におけるオメガ3脂肪酸の意義

    伊藤綾香, 小林アズサ, 白川伊吹, 菅波孝祥

    第62回日本脂質生化学会 

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    Event date: 2020.5

    Language:Japanese  

  21. Dietary supplementation of omega-3 fatty acid in mouse models of systemic lupus erythematosus

    Ito A, Kobyashi A, Suganami T

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    Event date: 2019.12

  22. Cholesterol accumulation in CD11c+ immune cells is a causal and targetable factor in autoimmune disease International coauthorship

    Ito A, Hong C, Oka K, Salazar JV, Diehl C, Witztum JL, Diaz M, Castrillo A, Bensinger SJ, Chan L, Tontonoz P

    The 47th Annual Meeting of the Japanese Society for Immunology  2018.12.11 

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    Event date: 2018.12

    Language:English   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  23. Molecular crosstalk between cholesterol metabolism and immune responses Invited International conference

    Ayaka Ito

    The 4th IMCR Symposium on endocrine and metabolism  2018.11.9 

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    Event date: 2018.11

    Language:English   Presentation type:Oral presentation (invited, special)  

    Venue:Gunma   Country:Japan  

  24. Molecular crosstalk between lipid metabolism and immune responses Invited International coauthorship

    Ito A, Hong C, Tontonoz P, Suganami T

    The 36th JES Summer Seminar Endocrinology & Metabolism  2018.8 

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    Event date: 2018.8

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Country:Japan  

  25. Cholesterol accumulation in CD11c+ immune cells is a causal and targetable factor in autoimmune disease International coauthorship International conference

    Ito A, Hong C, Oka K, Salazar JV, Diehl C, Witztum JL, Diaz M, Castrillo A, Bensinger SJ, Chan L, Tontonoz P

    Cell Symposia  2018.6 

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    Event date: 2018.6

    Language:English   Presentation type:Poster presentation  

    Venue:Basel   Country:Switzerland  

  26. Cellular cholesterol metabolism in autoimmune disease

    Ito A, Hong C, Tontonoz P, Suganami T

    The 91st Annual Meeting of the Japan Endocrine Society  2018.4 

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    Event date: 2018.4

    Language:Japanese   Presentation type:Oral presentation (general)  

  27. 自己免疫疾患発症における細胞内コレステロール代謝の意

    伊藤綾香、Cynthia Hong、Peter Tontonoz、菅波孝祥

    第55回日本臨床分子医学会学術集会  2018.4 

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    Event date: 2018.4

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Research Project for Joint Research, Competitive Funding, etc. 7

  1. 自己免疫疾患における多価不飽和脂肪酸代謝の意義の解明

    2023.4 - 2024.3

    公益財団法人日立財団 第54回(2022年度)倉田奨励金 

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    Authorship:Principal investigator 

    Grant amount:\1000000

  2. 免疫細胞内脂質に着目した全身エリテマトーデスの病態解明

    2021.4 - 2022.3

    公益財団法人稲盛財団 2021年度稲盛研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

  3. 細胞内脂質による免疫応答の制御機構と自己免疫疾患予防への応用

    2021 - 2023

    公益財団法人ロッテ財団 第8回(2021年度)奨励研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

  4. 細胞内脂質代謝に着目した自己免疫疾患の 新たな病態メカニズムの解明

    2020.4 - 2022.3

    公益財団法人加藤記念バイオサイエンス振興財団 第31回(2019年度)加藤記念研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

  5. 慢性炎症性疾患における細胞内脂質代謝の意義の解明

    2020.1 - 2020.12

    公益財団法人興和生命科学振興財団 2019年度研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

  6. 慢性炎症性疾患における脂質代謝の意義の解明

    2020 - 2022

    公益財団法人武田科学振興財団 2020年度ビジョナリーリサーチ継続助成(ホップ) 

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    Authorship:Principal investigator  Grant type:Competitive

  7. 慢性炎症性疾患における脂質代謝の意義の解明

    2019.11 - 2020.11

    花王健康科学研究会 第17回(2019年度)研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

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KAKENHI (Grants-in-Aid for Scientific Research) 12

  1. 脂質リモデリングから読み解く自己・非自己認識と治療への応用

    2023.4 - 2026.3

    創発的研究支援事業 

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    Authorship:Principal investigator 

  2. 免疫細胞内脂肪酸代謝の抗体産生における意義の解明

    Grant number:22K11700  2022.4 - 2025.3

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    伊藤 綾香

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    Authorship:Principal investigator 

    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

    自己免疫疾患は、自己抗体産生や炎症など免疫の過剰反応によって発症するが、その分子機構は未だに十分に理解されていない。従来の主流な治療法である非特異的な免疫療法は、結果としてウイルスや細菌に対する免疫応答低下を招き、感染症罹患などの致命的な問題となる事例が多い。本研究では自己免疫疾患の環境要因のひとつとして脂質代謝に着目し、自己に対する抗体と、感染時やワクチン接種時の抗体産生における脂質代謝の意義を解明する。
    自己免疫疾患は、自己抗体産生や炎症など、免疫の過剰反応によって発症するが、その分子機構は未だに十分に理解されていない。従来の主流な治療法である非特異的な免疫療法は、結果としてウイルスや細菌に対する免疫応答低下をもたらし、感染症罹患などの致命的な問題となる事例が多い。本研究では、自己免疫疾患の後天的要因のひとつとして脂質代謝に着目し、自己に対する抗体産生と、感染時の抗体産生における脂質代謝の意義を解明する。
    これまでに、免疫細胞の脂質蓄積が炎症生変化と自己免疫疾患の発症を促進すること、一方で細胞内コレステロールの減少や、オメガ3系多価不飽和脂肪酸の増加が、炎症や、B細胞から抗体産生細胞への分化を抑制し、病態を改善することを明らかにしてきた。現在、これらの脂質変化が感染時の抗体産生に及ぼす影響を検討している。また、免疫細胞における脂質と遺伝子発現の網羅的解析より、免疫細胞内の脂質代謝制御機構と、脂質による免疫応答制御機構の解明を試みている。本研究成果により、抗体産生における免疫細胞内脂質代謝の意義を解明し、自己免疫疾患の診断や治療に貢献したい。
    当該期間内に、脂質代謝遺伝子欠損マウスを用いて自己抗体産生および、外来抗原応答性抗体産生への影響を検討し、一定の成果を得ることができた。また、自己免疫疾患モデルマウスの血液サンプルを用いて脂質の網羅的解析を行い、病態関連脂質の候補となる脂質を挙げることができており、研究は概ね順調に進展していると言える。
    昨年度の引き続き、血中脂質解析から得られた、候補となる病態関連脂質についての詳細な解析を進める。既に報告されているヒト自己免疫疾患患者の血中解析データベースを用いた比較解析を行い、早期診断を可能とするような血中脂質マーカーの探索を行う。また、自己免疫疾患マウス、感染マウスより免疫細胞を単離して脂質解析、トランスクリプトーム解析を行うことにより、免疫細胞内の脂質代謝制御機構と、脂質による免疫応答制御機構を統合的に解明する。

  3. グリア内脂質代謝を介した脳-身体連関と末梢自己免疫応答制御の解明

    Grant number:21H05625  2021.9 - 2023.3

    科学研究費助成事業  学術変革領域研究(A)

    伊藤 綾香

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    Authorship:Principal investigator 

    Grant amount:\7800000 ( Direct Cost: \6000000 、 Indirect Cost:\1800000 )

    心理ストレスが末梢の生理機能を制御する「心身相関」は、経験的に知られているのもの、その実態は十分に理解されていない。代表的な自己免疫疾患である全身性エリテマトーデスは、全身に慢性炎症を呈する難病であり、その病態進展に伴い多彩な神経精神症状が生じる。一方、心理ストレスが自己免疫疾患の発症リスク増加や再燃に繋がることが報告されているが、そのメカニズムやミクログリアの関与は不明である。本研究では、心理ストレスによる末梢自己免疫応答制御のインターフェースとして、ミクログリアの脂質代謝に着目し、その病態生理的意義の解明を目指す。
    心理ストレスが末梢の生理機能を制御する「心身相関」は、経験的に知られているものの、その実態は十分に理解されていない。代表的な自己免疫疾患である全身性エリテマトーデスは、全身に慢性炎症を呈する難病であり、その病態進展に伴い多彩な神経精神症状が生じる。一方、心理ストレスが自己免疫疾患の発症リスク増加や再燃につながることが報告されているが、そのメカニズムやミクログリアの関与は不明である。本研究では、心理ストレスによる末梢自己免疫応答の制御のインターフェースとして、ミクログリアの脂質代謝に着目し、その病態整理的意義の解明を目指すことを目的とした。
    これまでに、心理ストレスモデルとして、マウスに社会的敗北ストレスおよび拘束ストレスを負荷し、末梢の免疫細胞、および脳内ミクログリアの動態を解析した。ストレス負荷により、T細胞やB細胞、好中球の数や割合に変化が生じること、特に好中球はいずれのストレスによっても増加する一方、その他の免疫細胞の動態は、ストレスの種類によって異なることが明らかとなった。また、薬剤によるミクログリア除去の検討から、ストレス負荷による全身性エリテマトーデス病態への影響の一部がミクログリア機能を介する可能性を示唆した。
    令和4年度が最終年度であるため、記入しない。
    令和4年度が最終年度であるため、記入しない。

  4. 慢性炎症性疾患の免疫細胞における脂質リプログラミングの意義の解明

    Grant number:19KK0249  2019.10 - 2024.3

    科学研究費助成事業  国際共同研究加速基金(国際共同研究強化(B))

    伊藤 綾香, 菅波 孝祥, 原 雄一郎

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\16770000 ( Direct Cost: \12900000 、 Indirect Cost:\3870000 )

    近年、種々の疾患に共通の基盤病態として慢性炎症が注目されているが、その分子機構は未だ十分に理解されておらず、特に免疫細胞内の脂質代謝異常の関与は不明である。本研究では、慢性炎症性の遷延化に伴う免疫細胞内脂質の量的・質的変化とその分子機構を明らかにする。また、自己免疫疾患と肥満を比較解析することにより、疾患特異的な、あるいは慢性炎症性疾患に共通の脂質リプログラミングの分子機構を解明し、治療標的としての可能性を検証する。本研究により、細胞内脂質代謝という従来にない切り口で疾患特異的な慢性炎症化の機構が明らかになるのみならず、慢性炎症性疾患の新しい診断・予防・治療の提案につながると期待される。
    近年、肥満や動脈硬化、自己免疫疾患など、種々の慢性疾患に共通の基盤病態として「慢性炎症」が注目されているが、その分子機構は未だ十分に理解されておらず、特に免疫細胞内の栄養代謝異常の関与は明らかにされていない。研究代表者はこれまでに、抗原提示細胞内の脂質蓄積が炎症、ひいては全身の自己免疫疾患を惹起することを明らかにし、病態の進展過程における免疫細胞内のダイナミックな脂質の質的・量的変化「脂質リプログラミング」の関与の可能性を示唆した。一方、肥満や非アルコール性脂肪肝炎など、過栄養により生じる全身性の慢性炎症に単球やマクロファージなどが関与することが報告されているが、全身の栄養代謝状態と免疫細胞内の栄養代謝状態の関係は分かっていない。
    現在までに、自己免疫疾患モデルマウスにおける多価不飽和脂肪酸の経口摂取が、炎症や、B細胞から抗体産生細胞への分化を抑制し、病態を改善することを明らかにした。また、病態における免疫細胞内の脂質および遺伝子発現の網羅的解析を行うことにより、病態の発症・進展に関与する脂質とその制御酵素を複数同定し、脂質代謝酵素の欠損マウスを用いることによって病態への影響を明らかにしつつある。本研究の成果により、細胞内脂質代謝という、従来にない切り口で慢性炎症性疾患のメカニズムが明らかになるのみならず、新しい診断・予防・治療の提案につながると期待される。
    当該期間内に、病態の発症・進展に関与する脂質とその制御酵素を複数同定し、脂質代謝酵素の欠損マウスを用いることによって病態への影響を明らかにしつつある。一方、当初予定していた解析、特に海外研究機関での解析について遅れが生じている。今年度、共同研究機関への渡航を予定しており、遅れている解析について進める予定である。
    シングルセルトランスクリプトーム解析とリピドーム解析を引き続き進めることにより、免疫細胞特異的な脂質の変化とその制御機構の解明を行う。また、現在解析中の脂質代謝酵素欠損マウスに関する結果を報告できるよう、引き続きの解析を進める。

  5. Quality and amount of lipid in autoimmune diseases

    Grant number:19K11765  2019.4 - 2022.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Ito Ayaka

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\4290000 ( Direct Cost: \3300000 、 Indirect Cost:\990000 )

    Accumulating evidence suggests that cholesterol accumulation in leukocytes is causally associated with the development of autoimmune diseases. However, the mechanism by which fatty acid composition influences autoimmune responses remains unclear. In this study, we found that dietary EPA supplementation ameliorated representative disease manifestations, including autoantibody production and immunocomplex deposition in the kidneys. A combination of lipidomic and membrane dynamics analyses revealed that EPA remodels the lipid composition and fluidity of B cell membranes, thereby preventing B cell differentiation into autoantibody-producing plasma cells. These results highlight a previously unrecognized mechanism by which fatty acid composition affects B cell differentiation into autoantibody-producing plasma cells during autoimmunity, and imply that EPA supplementation may be beneficial for therapy of autoimmune diseases.

  6. 細胞内脂肪酸の質に着目した自己免疫疾患発症の分子メカニズムの解明

    2018

    持田記念医学薬学振興財団  持田記念研究助成金 

    伊藤綾香

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    Authorship:Principal investigator  Grant type:Competitive

  7. Pathophysiological relevance of intracellular cholesterol metabolism in autoimmune diseases

    Grant number:17K16146  2017.4 - 2019.3

    Ito Ayaka

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

    In this study, we analyzed genetic and drug-induced SLE model mice and elucidated that titers of autoantibodies and deposition of immunoglobulin in kidney were increased in the SLE model mice compared to the control mice. We also found that lipid content in immune cells was higher in SLE than control mice, and which was observed at the beginning of the development of SLE. On the other hand, there was no difference in serum lipid profile and hepatic gene expression of lipid metabolism between SLE and control mice. Administration of an agent to improve systemic lipid metabolism prevented the development of SLE. These findings suggest that lipid accumulation in immune cells is cell intrinsic effect and improvement of systemic lipid metabolism could be beneficial in the setting of autoimmune disease.

  8. 自己免疫疾患発症における細胞内コレステロール代謝の病態生理的意義

    2017.4 - 2018.3

    日本学術振興会  科学研究費助成金 若手B 

    伊藤綾香

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    Authorship:Principal investigator  Grant type:Competitive

  9. 自己免疫疾患における細胞内コレステロール代謝の病態生理的意義の解明

    2017

    鈴木健三記念医科学応用研究財団  調査研究助成金 

    伊藤綾香

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    Authorship:Principal investigator  Grant type:Competitive

  10. 全身性エリテマトーデスにおける免疫細胞内リポクオリティの病態生理学的意義の解明

    2017

    小野医学研究財団  研究奨励助成 

    伊藤綾香

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    Authorship:Principal investigator  Grant type:Competitive

  11. 慢性炎症性疾患における脂質代謝の意義の解明

    2017

    武田科学振興財団  ビジョナリーリサーチ(スタート) 

    伊藤綾香

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    Authorship:Principal investigator  Grant type:Competitive

  12. 慢性炎症性疾患における脂質代謝の意義の解明

    2017

    アステラス病態代謝研究会  研究助成金 

    伊藤綾香

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    Authorship:Principal investigator  Grant type:Competitive

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Teaching Experience (On-campus) 4

  1. 環境学入門

    2023

  2. 自然科学と人間

    2021

  3. 自然科学と人間

    2020

  4. Studium Generale

    2019

Teaching Experience (Off-campus) 1

  1. 加齢学

    2019 Shigakkan University)

 

Social Contribution 23

  1. 2023年度 名古屋大学ホームカミングデイ「老いるオイルと老いないオイル」

    Role(s):Lecturer

    2023.10

  2. 中日健康フェア2023「おいしく楽しい身体づくり 〜生き生き健康的な食生活の秘訣とは?〜」

    Role(s):Lecturer

    中日健康フェア2023  2023.9

  3. 令和4年度・後期 岩倉市生涯学習講座「第6の栄養素・食物繊維と私たちの健康」

    Role(s):Lecturer

    2023.3

  4. 令和4年度・後期 岩倉市生涯学習講座「ビタミン・ミネラルと私たちの健康」

    Role(s):Lecturer

    2023.2

  5. 第54回 西三河糖尿病イブニングカンファランス「免疫代謝から考える糖尿病・メタボリックシンドロームと慢性炎症性疾患」

    Role(s):Lecturer

    2023.2

  6. 令和4年度・後期 岩倉市生涯学習講座「代謝って何?代謝の仕組みを知ってますます健康」

    Role(s):Lecturer

    2023.1

  7. 第88回名大カフェ"Science, and Me"「老いるオイルと老いないオイル」

    Role(s):Lecturer

    2022.9

  8. 名古屋市北生涯学習センター令和4年度前期講座「食を見直して安心・安全 〜普段の食生活を再点検〜」

    Role(s):Lecturer

    2022.6

  9. プレスリリース「エイコサペンタエン酸の摂取は形質細胞分化を抑制し、全身性エリテマトーデス病態を改善する」

    2022.6

  10. 名大ハカセの虫メガネ・みらいトーク特別企画「食と健康の未来」

    Role(s):Lecturer

    2022.5

  11. 国際ロータリー第2760地区例会「健康長寿の食生活」

    Role(s):Lecturer

    2022.5

  12. 中日新聞食育プロジェクト「いただきます!」

    Role(s):Commentator, Media coverage

    2022.4 - 2022.12

  13. CBCラジオ「未来につなげ 発見!日本の食」

    Role(s):Appearance, Commentator, Media coverage

    2022.4 - 2022.5

  14. Yamaoka Memorial Foundation, The 5th Science & Technology Lecture "Food as preventative medicine: Regulation of immune system by fermented food and nutrition"

    Role(s):Panelist, Lecturer

    2022.3

  15. 令和3年度・後期 岩倉市生涯学習講座「時間栄養学・体内時計に基づく健康的な食べ方」

    Role(s):Lecturer

    2022.3

  16. 令和3年度・後期 岩倉市生涯学習講座「塩の魅力と脅威」

    Role(s):Lecturer

    2022.2

  17. 令和3年度・後期 岩倉市生涯学習講座「タンパク質のはたらきと私たちの健康」

    Role(s):Lecturer

    2022.1

  18. 令和3年度在宅保健師会「あいち」第2回研修会「予防医学としての食を学ぶ・発酵食品のパワーと魅力」

    Role(s):Lecturer

    2021.10

  19. CBCラジオ「健康長寿の食」

    Role(s):Commentator

    2021.3

  20. 令和2年度・後期 岩倉市生涯学習講座「外出自粛時の食生活対策」

    Role(s):Lecturer

    2021.3

  21. 令和2年度・後期 岩倉市生涯学習講座「血管の欠陥」

    Role(s):Lecturer

    2021.2

  22. 令和2年度・後期 岩倉市生涯学習講座「感染症と免疫」

    Role(s):Lecturer

    2021.1

  23. CareTEX名古屋「認知症を予防する食事」

    Role(s):Lecturer

    2021.1

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