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42 results on '"Shimokawa, Chikako"'

3. Human Gut Microbiota and Its Metabolites Impact Immune Responses in COVID-19 and Its Complications

Author

Nagata, Naoyoshi, Takeuchi, Tadashi, Masuoka, Hiroaki, Aoki, Ryo, Ishikane, Masahiro, Iwamoto, Noriko, Sugiyama, Masaya, Suda, Wataru, Nakanishi, Yumiko, Terada-Hirashima, Junko, Kimura, Moto, Nishijima, Tomohiko, Inooka, Hiroshi, Miyoshi-Akiyama, Tohru, Kojima, Yasushi, Shimokawa, Chikako, Hisaeda, Hajime, Zhang, Fen, Yeoh, Yun Kit, Ng, Siew C., Uemura, Naomi, Itoi, Takao, Mizokami, Masashi, Kawai, Takashi, Sugiyama, Haruhito, Ohmagari, Norio, and Ohno, Hiroshi

Published
2023
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12. Queuine Is a Nutritional Regulator of Entamoeba histolytica Response to Oxidative Stress and a Virulence Attenuator

Author

Nagaraja, Shruti, primary, Cai, Maggi W., additional, Sun, Jingjing, additional, Varet, Hugo, additional, Sarid, Lotem, additional, Trebicz-Geffen, Meirav, additional, Shaulov, Yana, additional, Mazumdar, Mohit, additional, Legendre, Rachel, additional, Coppée, Jean-Yves, additional, Begley, Thomas J., additional, Dedon, Peter C., additional, Gourinath, Samudrala, additional, Guillen, Nancy, additional, Saito-Nakano, Yumiko, additional, Shimokawa, Chikako, additional, Hisaeda, Hajime, additional, and Ankri, Serge, additional

Published
2021
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15. Queuine is a nutritional regulator of Entamoeba histolytica response to oxidative stress and a virulence attenuator

Author

Nagaraja, Shruti, primary, Cai, Maggi W., additional, Sun, Jingjing, additional, Varet, Hugo, additional, Sarid, Lotem, additional, Trebicz-Geffen, Meirav, additional, Shaulov, Yana, additional, Mazumdar, Mohit, additional, Legendre, Rachel, additional, Coppée, Jean-Yves, additional, Begley, Thomas J., additional, Dedon, Peter C., additional, Gourinath, Samudrala, additional, Guillen, Nancy, additional, Saito-Nakano, Yumiko, additional, Shimokawa, Chikako, additional, Hisaeda, Hajime, additional, and Ankri, Serge, additional

Published
2020
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16. Fluctuations of Spleen Cytokine and Blood Lactate, Importance of Cellular Immunity in Host Defense Against Blood Stage Malaria Plasmodium yoelii

Author

Imai, Takashi, primary, Suzue, Kazutomo, additional, Ngo-Thanh, Ha, additional, Ono, Suguri, additional, Orita, Wakako, additional, Suzuki, Haruka, additional, Shimokawa, Chikako, additional, Olia, Alex, additional, Obi, Seiji, additional, Taniguchi, Tomoyo, additional, Ishida, Hidekazu, additional, Van Kaer, Luc, additional, Murata, Shigeo, additional, Tanaka, Keiji, additional, and Hisaeda, Hajime, additional

Published
2019
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21. Corrigendum: Plasmodium berghei ANKA causes intestinal malaria associated with dysbiosis

Author

Taniguchi, Tomoyo, Miyauchi, Eiji, Nakamura, Shota, Hirai, Makoto, Suzue, Kazutomo, Imai, Takashi, Nomura, Takahiro, Handa, Tadashi, Okada, Hiroko, Shimokawa, Chikako, Onishi, Risa, Olia, Alex, Hirata, Jun, Tomita, Haruyoshi, Ohno, Hiroshi, Horii, Toshihiro, and Hisaeda, Hajime

Subjects
DNA, Bacterial, Male, Mice, Inbred BALB C, Plasmodium berghei, Microbiota, Firmicutes, Corrigenda, Malaria, Intestines, Mice, Inbred C57BL, Feces, Mice, Blood-Brain Barrier, RNA, Ribosomal, 16S, Databases, Genetic, Proteobacteria, Animals, Dysbiosis
Abstract

Gastrointestinal symptoms, such as abdominal pain and diarrhea, are frequently observed in patients with Plasmodium falciparum malaria. However, the correlation between malaria intestinal pathology and intestinal microbiota has not been investigated. In the present study, infection of C57BL/6 mice with P. berghei ANKA (PbA) caused intestinal pathological changes, such as detachment of epithelia in the small intestines and increased intestinal permeability, which correlated with development with experimental cerebral malaria (ECM). Notably, an apparent dysbiosis occurred, characterized by a reduction of Firmicutes and an increase in Proteobacteria. Furthermore, some genera of microbiota correlated with parasite growth and/or ECM development. By contrast, BALB/c mice are resistant to ECM and exhibit milder intestinal pathology and dysbiosis. These results indicate that the severity of cerebral and intestinal pathology coincides with the degree of alteration in microbiota. This is the first report demonstrating that malaria affects intestinal microbiota and causes dysbiosis.

Published
2016

23. Correction: Corrigendum: Plasmodium berghei ANKA causes intestinal malaria associated with dysbiosis

Author

Taniguchi, Tomoyo, primary, Miyauchi, Eiji, additional, Nakamura, Shota, additional, Hirai, Makoto, additional, Suzue, Kazutomo, additional, Imai, Takashi, additional, Nomura, Takahiro, additional, Handa, Tadashi, additional, Okada, Hiroko, additional, Shimokawa, Chikako, additional, Onishi, Risa, additional, Olia, Alex, additional, Hirata, Jun, additional, Tomita, Haruyoshi, additional, Ohno, Hiroshi, additional, Horii, Toshihiro, additional, and Hisaeda, Hajime, additional

Published
2016
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24. Plasmodium berghei ANKA causes intestinal malaria associated with dysbiosis

Author

Taniguchi, Tomoyo, primary, Miyauchi, Eiji, additional, Nakamura, Shota, additional, Hirai, Makoto, additional, Suzue, Kazutomo, additional, Imai, Takashi, additional, Nomura, Takahiro, additional, Handa, Tadashi, additional, Okada, Hiroko, additional, Shimokawa, Chikako, additional, Onishi, Risa, additional, Olia, Alex, additional, Hirata, Jun, additional, Tomita, Haruyoshi, additional, Ohno, Hiroshi, additional, Horii, Toshihiro, additional, and Hisaeda, Hajime, additional

Published
2015
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28. Medical Professionals' Perceptions of the Effect of Pharmacist Interventions in Care for HIV Patients

Author

Kunimoto, Yusuke, primary, Yoshino, Munehiro, additional, Ohishi, Yuki, additional, Harada, Sachiko, additional, Inoue, Masatomo, additional, Sato, Maki, additional, Uchiyama, Mariko, additional, Saito, Naomi, additional, Maruyama, Ichiro, additional, Shimokawa, Chikako, additional, Unei, Hiroko, additional, Matsumoto, Shunji, additional, Masuda, Junichi, additional, Chida, Masayuki, additional, Izumi, Keishiro, additional, and Miyamoto, Atsushi, additional

Published
2014
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35. Development of experimental cerebral malaria is independent of IL-23 and IL-17

Author

Ishida, Hidekazu, primary, Matsuzaki-Moriya, Chikako, additional, Imai, Takashi, additional, Yanagisawa, Kunio, additional, Nojima, Yoshihisa, additional, Suzue, Kazutomo, additional, Hirai, Makoto, additional, Iwakura, Yoichiro, additional, Yoshimura, Akihiko, additional, Hamano, Shinjiro, additional, Shimokawa, Chikako, additional, and Hisaeda, Hajime, additional

Published
2010
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38. IL-23 protection against Plasmodium berghei infection in mice is partially dependent on IL-17 from macrophages.

Author

Ishida, Hidekazu, Imai, Takashi, Suzue, Kazutomo, Hirai, Makoto, Taniguchi, Tomoyo, Yoshimura, Akihiko, Iwakura, Yoichiro, Okada, Hiroko, Suzuki, Tomohisa, Shimokawa, Chikako, and Hisaeda, Hajime

Abstract

Although IL-12 is believed to contribute to protective immune responses, the role played by IL-23 (a member of the IL-12 family) in malaria is elusive. Here, we show that IL-23 is produced during infection with Plasmodium berghei NK65. Mice deficient in IL-23 (p19 KO) had higher parasitemia and died earlier than wild-type ( WT) controls. Interestingly, p19 KO mice had lower numbers of IL-17-producing splenic cells than their WT counterparts. Furthermore, mice deficient in IL-17 (17 KO) suffered higher parasitemia than the WT controls, indicating that IL-23-mediated protection is dependent on induction of IL-17 during infection. We found that macrophages were responsible for IL-17 production in response to IL-23. We observed a striking reduction in splenic macrophages in the p19 KO and 17 KO mice, both of which became highly susceptible to infection. Thus, IL-17 appears to be crucial for maintenance of splenic macrophages. Adoptive transfer of macrophages into macrophage-depleted mice confirmed that macrophage-derived IL-17 is required for macrophage accumulation and parasite eradication in the recipient mice. We also found that IL-17 induces CCL2/7, which recruit macrophages. Our findings reveal a novel protective mechanism whereby IL-23, IL-17, and macrophages reduce the severity of infection with blood-stage malaria parasites. [ABSTRACT FROM AUTHOR]

Published
2013
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39. Involvement of CD8.

Author

Imai, Takashi, Shen, Jianying, Chou, Bin, Duan, Xuefeng, Tu, Liping, Tetsutani, Kohhei, Moriya, Chikako, Ishida, Hidekazu, Hamano, Shinjiro, Shimokawa, Chikako, Hisaeda, Hajime, and Himeno, Kunisuke

Abstract

When developing malaria vaccines, the most crucial step is to elucidate the mechanisms involved in protective immunity against the parasites. We found that CD8 T cells contribute to protective immunity against infection with blood-stage parasites of Plasmodium yoelii. Infection of C57BL/6 mice with P. yoelii 17XL was lethal, while all mice infected with a low-virulence strain of the parasite 17XNL acquired complete resistance against re-infection with P. yoelii 17XL. However, the host mice transferred with CD8 T cells from mice primed only with P. yoelii 17XNL failed to acquire protective immunity. On the other hand, the irradiated host mice were completely resistant to P. yoelii 17XL infection, showing no grade of parasitemia when adoptively transferred with CD8 T cells from immune mice that survived infection with both P. yoelii XNL and, subsequently, P. yoelii 17XL. These protective CD8 T cells from immune WT mice had the potential to generate IFN-γ, perforin (PFN) and granzyme B. When mice deficient in IFN-γ were used as donor mice for CD8 T cells, protective immunity in the host mice was fully abrogated, and the immunity was profoundly attenuated in PFN-deficient mice. Thus, CD8 T cells producing IFN-γ and PFN appear to be involved in protective immunity against infection with blood-stage malaria. [ABSTRACT FROM AUTHOR]

Published
2010
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40. Queuine Is a Nutritional Regulator of Entamoeba histolyticaResponse to Oxidative Stress and a Virulence Attenuator

Author

Nagaraja, Shruti, Cai, Maggi W., Sun, Jingjing, Varet, Hugo, Sarid, Lotem, Trebicz-Geffen, Meirav, Shaulov, Yana, Mazumdar, Mohit, Legendre, Rachel, Coppée, Jean-Yves, Begley, Thomas J., Dedon, Peter C., Gourinath, Samudrala, Guillen, Nancy, Saito-Nakano, Yumiko, Shimokawa, Chikako, Hisaeda, Hajime, and Ankri, Serge

Abstract

Entamoeba histolyticais a unicellular parasite that causes amebiasis. The parasite resides in the colon and feeds on the colonic microbiota.

Published
2021
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41. Species-Specific Immunity Induced by Infection with Entamoeba histolytica and Entamoeba moshkovskii in Mice.

Author

Shimokawa, Chikako, Culleton, Richard, Imai, Takashi, Suzue, Kazutomo, Hirai, Makoto, Taniguchi, Tomoyo, Kobayashi, Seiki, Hisaeda, Hajime, and Hamano, Shinjiro

Subjects
*ENTAMOEBA histolytica, *AMEBIASIS, *PARASITIC diseases, *DEATH rate, *TROPHOZOITES, *METRONIDAZOLE, *IMMUNE response, *LABORATORY mice
Abstract

Entamoeba histolytica, the parasitic amoeba responsible for amoebiasis, causes approximately 100,000 deaths every year. There is currently no vaccine against this parasite. We have previously shown that intracecal inoculation of E. histolytica trophozoites leads to chronic and non-healing cecitis in mice. Entamoeba moshkovskii, a closely related amoeba, also causes diarrhea and other intestinal disorders in this model. Here, we investigated the effect of infection followed by drug-cure of these species on the induction of immunity against homologous or heterologous species challenge. Mice were infected with E. histolytica or E. moshkovskii and treated with metronidazole 14 days later. Re-challenge with E. histolytica or E. moshkovskii was conducted seven or 28 days following confirmation of the clearance of amoebae, and the degree of protection compared to non-exposed control mice was evaluated. We show that primary infection with these amoebae induces a species-specific immune response which protects against challenge with the homologous, but not a heterologous species. These findings pave the way, therefore, for the identification of novel amoebae antigens that may become the targets of vaccines and provide a useful platform to investigate host protective immunity to Entamoeba infections. [ABSTRACT FROM AUTHOR]

Published
2013
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42. Involvement of CD8+ T cells in protective immunity against murine blood-stage infection with Plasmodium yoelii 17XL strain.

Author

Imai T, Shen J, Chou B, Duan X, Tu L, Tetsutani K, Moriya C, Ishida H, Hamano S, Shimokawa C, Hisaeda H, and Himeno K

Subjects
Adoptive Transfer, Animals, CD8-Positive T-Lymphocytes metabolism, CD8-Positive T-Lymphocytes transplantation, Convalescence, DNA-Binding Proteins deficiency, DNA-Binding Proteins genetics, Female, Granzymes biosynthesis, Interferon-gamma biosynthesis, Interferon-gamma deficiency, Interferon-gamma genetics, Macrophages immunology, Malaria prevention & control, Malaria Vaccines immunology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Parasitemia prevention & control, Plasmodium yoelii pathogenicity, Pore Forming Cytotoxic Proteins biosynthesis, Pore Forming Cytotoxic Proteins deficiency, Pore Forming Cytotoxic Proteins genetics, Radiation Chimera, Virulence, CD8-Positive T-Lymphocytes immunology, Malaria immunology, Parasitemia immunology, Plasmodium yoelii immunology
Abstract

When developing malaria vaccines, the most crucial step is to elucidate the mechanisms involved in protective immunity against the parasites. We found that CD8(+) T cells contribute to protective immunity against infection with blood-stage parasites of Plasmodium yoelii. Infection of C57BL/6 mice with P. yoelii 17XL was lethal, while all mice infected with a low-virulence strain of the parasite 17XNL acquired complete resistance against re-infection with P. yoelii 17XL. However, the host mice transferred with CD8(+) T cells from mice primed only with P. yoelii 17XNL failed to acquire protective immunity. On the other hand, the irradiated host mice were completely resistant to P. yoelii 17XL infection, showing no grade of parasitemia when adoptively transferred with CD8(+) T cells from immune mice that survived infection with both P. yoelii XNL and, subsequently, P. yoelii 17XL. These protective CD8(+) T cells from immune WT mice had the potential to generate IFN-gamma, perforin (PFN) and granzyme B. When mice deficient in IFN-gamma were used as donor mice for CD8(+) T cells, protective immunity in the host mice was fully abrogated, and the immunity was profoundly attenuated in PFN-deficient mice. Thus, CD8(+) T cells producing IFN-gamma and PFN appear to be involved in protective immunity against infection with blood-stage malaria.

Published
2010
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