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Published Papers 【 display / non-display 】

• <i>Babesia microti</i> alleviates disease manifestations caused by <i>Plasmodium berghei</i> ANKA in murine co-infection model of complicated malaria

  Zafar, I; Taniguchi, T; Baghdadi, HB; Kondoh, D; Rizk, MA; Galon, EM; Ji, SW; El-Sayed, SA; Do, T; Li, H; Amer, MM; Ma, ZW; Ma, YH; Zhou, JL; Inoue, N; Xuan, XA

  FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY ( Frontiers in Cellular and Infection Microbiology )  13   1226088 - 1226088   2023.07 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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  Malaria remains one of the most significant health issues worldwide, accounting for 2.6% of the total global disease burden, and efforts to eliminate this threat continue. The key focus is to develop an efficient and long-term immunity to this disease via vaccination or therapeutic approach, and innovative strategies would enable us to achieve this target. Previously, using a mouse co-infection disease model, cross-protection was illustrated between Babesia microti and Plasmodium chabaudi. Hence, this study was planned to elucidate the impact of acute B. microti Peabody mjr and Plasmodium berghei ANKA co-infection on the consequence of complicated malaria in the C57BL/6J mouse model of malaria. Furthermore, immune response and pathological features were analyzed, and the course of the disease was compared among experimental groups. Our study established that acute B. microti infection activated immunity which was otherwise suppressed by P. berghei. The immunosuppressive tissue microenvironment was counteracted as evidenced by the enhanced immune cell population in co-infected mice, in contrast to P. berghei-infected control mice. Parasite sequestration in the brain, liver, lung, and spleen of co-infected mice was significantly decreased and tissue injury was ameliorated. Meanwhile, the serum levels of IFN-γ, TNF-α, and IL-12p70 were reduced while the secretion of IL-10 was promoted in co-infected mice. Eventually, co-infected mice showed an extended rate of survival. Hereby, the principal cytokines associated with the severity of malaria by P. berghei infection were TNF-α, IFN-γ, and IL-12p70. Moreover, it was evident from our flow cytometry results that innate immunity is crucial and macrophages are at the frontline of immunity against P. berghei infection. Our study recommended further investigations to shed light on the effects of babesiosis in suppressing malaria with the goal of developing Babesia-based therapy against malaria.

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• Effect of α-Tocopheryloxy Acetic Acid on the Infection of Mice with Plasmodium berghei ANKA In Vivo and Humans with P. falciparum In Vitro.

  Nanang R Ariefta, Aiko Kume, Yoshifumi Nishikawa, Tomoyo Taniguchi, Rika Umemiya-Shirafuji, Shunji Kasai, Hiroshi Suzuki

  Acta parasitologica     2022.08 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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  PURPOSE: Malarial parasites are susceptible to oxidative stress. The effects of α-tocopheryloxy acetic acid (α-TEA), a vitamin E analog, on infection by Plasmodium berghei ANKA and P. falciparum in mice and human red blood cells (RBCs), respectively, were examined in this study. METHODS: For in vivo studies in mice, RBCs infected with P. berghei ANKA were inoculated via intraperitoneal injection and α-TEA was administered to C57BL/6 J male mice after infection. The blood-brain barrier (BBB) permeability was examined by Evans blue staining in experimental cerebral malaria at 7 days after infection. The in vitro inhibitory effect of α-TEA on P. falciparum 3D7 (chloroquine-sensitive strain) and K1 (multidrug-resistant strain) was tested using a SYBR Green I-based assay. RESULTS: When 1.5% α-TEA was administered for 14 days after infection, 88% of P. berghei ANKA-infected mice survived during the experimental period. Nevertheless, all the control mice died within 12 days of infection. Furthermore, the Evans blue intensity in α-TEA-treated mice brains was less than that in untreated mice, indicating that α-TEA might inhibit the destruction of the BBB and progression of cerebral malaria. The in vitro experiment revealed that α-TEA inhibited the proliferation of both the 3D7 and K1 strains. CONCLUSION: This study showed that α-TEA is effective against murine and human malaria in vivo and in vitro, respectively. Although α-TEA alone has a sufficient antimalarial effect, future research could focus on the structure-activity relationship to achieve better pharmacokinetics and decrease the cytotoxicity and/or the combined effect of α-TEA with existing drugs. In addition, the prophylactic antimalarial activity of premedication with α-TEA may also be an interesting perspective in the future.

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• The role of autonomously secreted PGE2 and its autocrine/paracrine effect on bone matrix mineralization at the different stages of differentiating MC3T3-E1 cells.

  Hiraku Suzuki, Noriyasu Ohshima, Kazuaki Tatei, Tomoyo Taniguchi, Seiichi Sato, Takashi Izumi

  Biochemical and biophysical research communications   524 ( 4 ) 929 - 935   2020.04 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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  Bone is consisted of osteoblast-linage cells, bone-forming cells in various differentiation stages. However, it is not fully understood how communicate and interact these cells immigrated from bone marrow. In this study, we showed that prostaglandin E2 (PGE2) had a role in autonomous modification of matrix mineralization in osteoblastic cell line, MC3T3-E1, and interactions across the cells in different differentiation stages. Analysis using LC-MS/MS and inhibitors showed the autonomous secretion of PGE2 among the prostanoids in differentiation stages and that depend on COX-2, a key enzyme for production of PGE2. Treatment with inhibitors of PGE2 receptors and COX-2 indicated that secreted PGE2 regulates matrix mineralization in an autocrine/paracrine manner. In addition, we showed that the expression profile of PGE2 receptors (EP1-EP4) and PGE2 effects on matrix mineralization derived from it changed during cell differentiation. Treatment with inhibitors of PGE2 signaling in the early differentiation stage of MC3T3-E1 cells induced significant changes in matrix mineralization several days after. Stimulation with the extracts from culture medium of the matured cells including PGE2 and co-culture with the matured cells secreting PGE2 significantly promoted matrix mineralization of the early stage cells, in contrast, treatment with inhibitor of COX-2 and PGE2 receptors failed to do so. These results support that PGE2 plays important roles in the interaction system of osteoblast-linage cells in bone tissue to regulate matrix mineralization reflecting condition of bone-forming cells, that is, population and maturation.

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• Fluctuations of Spleen Cytokine and Blood Lactate, Importance of Cellular Immunity in Host Defense Against Blood Stage Malaria <i>Plasmodium yoelii</i>.

  Imai T, Suzue K, Ngo-Thanh H, Ono S, Orita W, Suzuki H, Shimokawa C, Olia A, Obi S, Taniguchi T, Ishida H, Van Kaer L, Murata S, Tanaka K, Hisaeda H

  Frontiers in immunology   10   2207 - 2207   2019 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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  Our previous studies of protective immunity and pathology against blood stage malaria parasites have shown that not only CD4+ T cells, but also CD8+ T cells and macrophages, are important for host defense against blood stage malaria infection. Furthermore, we found that Plasmodium yoelii 17XNL (PyNL) parasitizes erythroblasts, the red blood cell (RBC) precursor cells, which then express MHC class I molecules. In the present study, we analyzed spleen cytokine production. In CD8+ T cell-depleted mice, IL-10 production in early stage infection was increased over two-fold relative to infected control animals and IL-10+ CD3- cells were increased, whereas IFN-γ production in the late stage of infection was decreased. At day 16 after PyNL infection, CD8+ T cells produced more IFN-γ than CD4+ T cells. We evaluated the involvement of the immunoproteasome in induction of immune CD8+ T cells, and the role of Fas in protection against PyNL both of which are downstream of IFN-γ. In cell transfer experiments, at least the single molecules LMP7, LMP2, and PA28 are not essential for CD8+ T cell induction. The Fas mutant LPR mouse was weaker in resistance to PyNL infection than WT mice, and 20% of the animals died. LPR-derived parasitized erythroid cells exhibited less externalization of phosphatidylserine (PS), and phagocytosis by macrophages was impaired. Furthermore, we tried to identify the cause of death in malaria infection. Blood lactate concentration was increased in the CD8+ T cell-depleted PyNL-infected group at day 19 (around peak parasitemia) to similar levels as day 7 after infection with a lethal strain of Py. When we injected mice with lactate at day 4 and 6 of PyNL infection, all mice died at day 8 despite demonstrating low parasitemia, suggesting that hyperlactatemia is one of the causes of death in CD8+ T cell-depleted PyNL-infected mice. We conclude that CD8+ T cells might control cytokine production to some extent and regulate hyperparasitemia and hyperlactatemia in protection against blood stage malaria parasites.

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• A possible origin population of pathogenic intestinal nematodes, Strongyloides stercoralis, unveiled by molecular phylogeny

  Eiji Nagayasu, Myo Pa Pa Thet Hnin Htwe Aung, Thanaporn Hortiwakul, Akina Hino, Teruhisa Tanaka, Miwa Higashiarakawa, Alex Olia, Tomoyo Taniguchi, Soe Moe Thu Win, Isao Ohashi, Emmanuel Igwaro Odongo-Aginya, Khin Myo Aye, Mon Mon, Kyu Kyu Win, Kei Ota, Yukari Torisu, Siripen Panthuwong, Eisaku Kimura, Nirianne M. Q. Palacpac, Taisei Kikuchi, Tetsuo Hirata, Shidow Torisu, Hajime Hisaeda, Toshihiro Horii, Jiro Fujita, Wah Win Htike, Haruhiko Maruyama

  SCIENTIFIC REPORTS ( NATURE PUBLISHING GROUP )  7 ( 1 ) 4844   2017.07 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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  Humans and dogs are the two major hosts of Strongyloides stercoralis, an intestinal parasitic nematode. To better understand the phylogenetic relationships among S. stercoralis isolates infecting humans and dogs and to assess the zoonotic potential of this parasite, we analyzed mitochondrial Cox1, nuclear 18S rDNA, 28S rDNA, and a major sperm protein domain-containing protein genes. Overall, our analyses indicated the presence of two distinct lineages of S. stercoralis (referred to as type A and type B). While type A parasites were isolated both from humans and dogs in different countries, type B parasites were found exclusively in dogs, indicating that the type B has not adapted to infect humans. These epidemiological data, together with the close phylogenetic relationship of S. stercoralis with S. procyonis, a Strongyloides parasite of raccoons, possibly indicates that S. stercoralis originally evolved as a canid parasite, and later spread into humans. The inability to infect humans might be an ancestral character of this species and the type B might be surmised to be an origin population from which human-infecting strains are derived.

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Books 【 display / non-display 】

Books 【 display / non-display 】

• Gastrointestinal symptoms and microbiota during malaria infection

  TANIGUCHI Tomoyo ( Part: Single Author )

  Clinical immunology & allergology  2018.01

Other Papers 【 display / non-display 】

Other Papers 【 display / non-display 】

• ウガンダ国の熱帯熱マラリア患者において腸内細菌叢の変化が起こる

  谷口 委代, 宮内 栄治, Olia Alex, 長安 英治, Osbert Katuro, 鈴江 一友, 今井 孝, 下川 周子, 大西 里咲, Odongo-Aginya E.I, Palacpac Nirianne, 丸山 治彦, 木村 英作, 美田 敏宏, 大野 博司, 堀井 俊宏, 久枝 一

  グローバルヘルス合同大会プログラム・抄録集 ( グローバルヘルス合同大会事務局 )  2017   192 - 192   2017.11  [Refereed]

   

Presentations 【 display / non-display 】

Presentations 【 display / non-display 】

• Plasmodium berghei ANKA infected C57BL/6N mice suffer from pathological lesions and lymphopenia in the intestine

  Taniguchi T, Hasunuma M, Ikezawa I, Saitoh J, Toma H, Suzuki H, Hisaeda H, Kishimoto H

  第52回日本免疫学会学術集会  2024.01  -  2024.01 

• Gut microbiota and malarial pathology in C57BL/6N mice with ameliorated experimental cerebral malaria

  Tomoyo Taniguchi, Eiji Miyauchi, Reika Kawabata-Iwakawa, Masahiko Nishiyama, Rika Umemiya-Shirafuji, Hiromu Toma, Hajime Hisaeda, Hidehiro Kishimoto, Hiroshi Ohno, Haruyoshi Tomita, Hiroshi Suzuki

  The 9th International Human Microbiome Consortium Congress 2022 KOBE (IHMC2022)  2022.11  -  2022.11 

• A unique subset of γδ T cells expands and produces IL-10 in patients with naturally acquired immunity against Falciparum Malaria

  1900.01  -  1900.01 

• Altered gut microbiota by antibiotics administration ameliorates experimental cerebral malaria in C57BL/6N mice

  Taniguchi T, Miyauchi E, Kawabata-Iwakawa R, Nishiyama M, Umemiya-Shirafuji R, Hisaeda H, Ohno H, Tomita H, Suzuki H

  15th International Congress of Parasitology  1900.01  -  1900.01 

• Altered gut microbiota composition in patients with Plasmodium falciparum malaria

  Eiji Miyauchi, Tomoyo Taniguchi, Alex Olia, Eiji Nagayasu, Katuro Osbert, Kazutomo Suzue, Takashi Imai, Chikako Shimokawa, Risa Onishi, E.I. Odongo-Aginya, Nirianne Palacpac, Haruhiko Maruyama, Eisaku Kimura, Toshihiro Mita, Toshihiro Horii, Hajime Hisaeda, Hiroshi Ohno

  1900.01  -  1900.01 

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Academic Awards 【 display / non-display 】

Academic Awards 【 display / non-display 】

• Travel Award for International Congress of Parasitology 2018

  2018.06   Japanese Society of Parasitology  

  Winner: TANIGUCHI Tomoyo

Grant-in-Aid for Scientific Research 【 display / non-display 】

Grant-in-Aid for Scientific Research 【 display / non-display 】

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

  Project Year: 2023.04  -  2026.03 

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

  Project Year: 2023.04  -  2026.03 

  Direct: 3,600,000 (YEN)  Overheads: 4,680,000 (YEN)  Total: 1,080,000 (YEN)

• Grant-in-Aid for JSPS Fellows

  Project Year: 2020.04  -  2023.03 

  Direct: 3,700,000 (YEN)  Overheads: 4,810,000 (YEN)  Total: 1,110,000 (YEN)

• Grant-in-Aid for JSPS Fellows

  Project Year: 2020.04  -  2023.03 

  Direct: 3,700,000 (YEN)  Overheads: 4,810,000 (YEN)  Total: 1,110,000 (YEN)

• Grant-in-Aid for Young Scientists(B)

  Project Year: 2016.04  -  2020.03 

  Direct: 0 (YEN)  Overheads: 0 (YEN)  Total: 0 (YEN)

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Other External funds 【 display / non-display 】

Other External funds 【 display / non-display 】

• Project Year: 2023.04  -  2025.03 

  Offer Organization: Takahashi Industrial and Economic Research Foundation

SDGs 【 display / non-display 】

SDGs 【 display / non-display 】