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Your search keyword '"Shimokawa, Chikako"' showing total 4 results
Start Over Author "Shimokawa, Chikako" Publisher nature publishing group
4 results on '"Shimokawa, Chikako"'

1. 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

3. Plasmodium berghei ANKA causes intestinal malaria associated with dysbiosis.

Author

Taniguchi T, Miyauchi E, Nakamura S, Hirai M, Suzue K, Imai T, Nomura T, Handa T, Okada H, Shimokawa C, Onishi R, Olia A, Hirata J, Tomita H, Ohno H, Horii T, and Hisaeda H

Subjects
Animals, Blood-Brain Barrier metabolism, DNA, Bacterial analysis, DNA, Bacterial isolation & purification, Databases, Genetic, Feces microbiology, Firmicutes genetics, Firmicutes isolation & purification, Intestines pathology, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Microbiota, Proteobacteria genetics, Proteobacteria isolation & purification, RNA, Ribosomal, 16S analysis, RNA, Ribosomal, 16S genetics, RNA, Ribosomal, 16S metabolism, Dysbiosis etiology, Intestines microbiology, Malaria complications, Malaria pathology, Plasmodium berghei physiology
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
2015
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4. CD8(+) T cell activation by murine erythroblasts infected with malaria parasites.

Author

Imai T, Ishida H, Suzue K, Hirai M, Taniguchi T, Okada H, Suzuki T, Shimokawa C, and Hisaeda H

Subjects
Animals, Erythroblasts immunology, Green Fluorescent Proteins genetics, Histocompatibility Antigens Class I immunology, Histocompatibility Antigens Class I metabolism, Malaria parasitology, Mice, Mice, Inbred C57BL, Mice, Knockout, Ovalbumin genetics, Ovalbumin immunology, CD8-Positive T-Lymphocytes immunology, Erythroblasts parasitology, Lymphocyte Activation immunology, Malaria immunology, Plasmodium yoelii immunology
Abstract

Recent studies show that some human malaria parasite species Plasmodium falciparum and P. vivax parasitize erythroblasts; however, the biological and clinical significance of this is unclear. To investigate further, we generated a rodent malaria parasite (P. yoelii 17XNL) expressing GFP-ovalbumin (OVA). Its infectivity to erythroblasts was confirmed, and parasitized erythroblasts were capable of initiating malaria infections. Experiments showed that MHC class I molecules were highly expressed on parasitized erythroblasts. As CD8(+) T cells recognize MHC class I and peptide complexes on target cells, and are involved in protection or pathology against malaria, we examined whether erythroblasts are targeted by CD8(+) T cells. Purified non-parasitized erythroblasts pulsed with OVA peptides were recognized by OVA-specific CD8(+) T cells. Crucially, parasitized erythroblasts isolated from GFP-OVA-, but not GFP- infected-mice, activated OT-I CD8(+) T cells, indicating that CD8(+) T cells recognize parasitized erythroblasts in an antigen-specific manner.

Published
2013
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