Browsing by Author "Daisuke Motooka"

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    BATF2 prevents T-cell-mediated intestinal inflammation through regulation of the IL-23/IL-17 pathway
    (2019-02-19) Hisako Kayama; Haruka Tani; Shoko Kitada; Anunya Opasawatchai; Ryu Okumura; Daisuke Motooka; Shota Nakamura; Kiyoshi Takeda; Osaka University; Japan Science and Technology Agency; Mahidol University
    © The Japanese Society for Immunology. 2019. All rights reserved. Inappropriate activation of the IL-23 signaling pathway causes chronic inflammation through the induction of immunopathological Th17 cells in several tissues including the intestine, whereas adequate Th17 responses are essential for host defense against harmful organisms. In the intestinal lamina propria, IL-23 is primarily produced by innate myeloid cells including dendritic cells (DCs) and macrophages (M?s). However, the molecular mechanisms underlying the regulation of IL-23 production by these cells remains poorly understood. In this study, we demonstrated that BATF2 regulates intestinal homeostasis by inhibiting IL-23-driven T-cell responses. Batf2 was highly expressed in intestinal innate myeloid subsets, such as monocytes, CD11b+ CD64+ M?s and CD103+ DCs. Batf2-/- mice spontaneously developed colitis and ileitis with altered microbiota composition. In this context, IL-23, but not TNF-a and IL-10, was produced in high quantities by intestinal CD11b+ CD64+ M?s from Batf2-/- mice compared with wild-type mice. Moreover, increased numbers of IFN-?+, IL-17+ and IFN-?+ IL-17+ CD4+ T cells, but not IL-10+ CD4+ T cells, accumulated in the colons and small intestines of Batf2-/- mice. In addition, ROR?t-expressing innate lymphoid cells were increased in Batf2-/- mice. Batf2-/- Rag2-/- mice showed a reduction in intestinal inflammation present in Batf2-/- mice. Furthermore, the high numbers of intestinal IL-17+ and IFN-?+ IL-17+ CD4+ T cells were markedly reduced in Batf2-/- mice when introducing Il23a deficiency, which was associated with the abrogation of intestinal inflammation. These results indicated that BATF2 in innate myeloid cells is a key molecule for the suppression of IL-23/IL-17 pathway-mediated adaptive intestinal pathology.
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    Corrigendum to “Plasmid dynamics in Vibrio parahaemolyticus strains related to shrimp Acute Hepatopancreatic Necrosis Syndrome (AHPNS)” [Infect. Genet. Evol. (2017) 51: 211–218] (S156713481730120X) (10.1016/j.meegid.2017.04.007))
    (2018-01-01) Chonchanok Theethakaew; Shota Nakamura; Daisuke Motooka; Shigeaki Matsuda; Toshio Kodama; Kaknokrat Chonsin; Orasa Suthienkul; Tetsuya Iida; Rajabhat University; Osaka University; Mahidol University; Thammasat University
    © 2017 Elsevier B.V. The authors regret to inform that there were two errors in the affiliation of a collaborator (Materials and Methods) and grant information (Acknowledgment). 1. Materials and methods: (Error text). Dr. Timothy W. Flegal (National Research Council of Thailand and National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Thailand). (Correction). Prof. Timothy W. Flegel (Thai National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency). 2. Acknowledgement: (Error text). Bacterial strain VP2HP used in this research was derived from a previous project that was funded by National Research Council of Thailand (Project code no. 54801) and supported by Dr. Kallaya Sritunyalucksana-Dangtip. (Correction). Bacterial isolate 2HP used in this study has been achieved from the project granted by the National Research Council of Thailand (Project code no. 54801) to K. Sritunyalucksana (Thailand National Center for Genetic Engineering and Biotechnology). The authors would like to apologise for any inconvenience caused.
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    Genomic characterization of carbapenemase-producing klebsiella pneumoniae with chromosomally carried bla NDM-1
    (2018-12-01) Noriko Sakamoto; Yukihiro Akeda; Yo Sugawara; Dan Takeuchi; Daisuke Motooka; Norihisa Yamamoto; Warawut Laolerd; Pitak Santanirand; Shigeyuki Hamada; Osaka University; Handai Byoin; Faculty of Medicine, Ramathibodi Hospital, Mahidol University
    © 2018 American Society for Microbiology. All Rights Reserved. We report here Klebsiella pneumoniae strains carrying chromosomal bla NDM-1 in Thailand. The genomes of these two isolates include a 160-kbp insertion containing bla NDM-1 , which is almost identical to that in the IncHI1B-like plasmid. Further analysis indicated that IS5-mediated intermolecular transposition and Tn3 transposase-mediated homologous recombination resulted in the integration of bla NDM-1 into the chromosome from an IncHI1B-like plasmid. The spread of this type of carbapenem-resistant Enterobacteriaceae may threaten public health and warrants further monitoring.
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    Plasmid dynamics in Vibrio parahaemolyticus strains related to shrimp Acute Hepatopancreatic Necrosis Syndrome (AHPNS)
    (2017-07-01) Chonchanok Theethakaew; Shota Nakamura; Daisuke Motooka; Shigeaki Matsuda; Toshio Kodama; Kaknokrat Chonsin; Orasa Suthienkul; Tetsuya Iida; Mahidol University; Osaka University; Rajabhat University; Thammasat University
    © 2017 Elsevier B.V. Vibrio parahaemolyticus is a causative agent of acute hapatopancreatic necrosis syndrome (AHPNS) which causes early mortality in white shrimp. Emergence of AHPNS has caused tremendous economic loss for aquaculture industry particularly in Asia since 2010. Previous studies reported that strains causing AHPNS harbor a 69-kb plasmid with possession of virulence genes, pirA and pirB. However, genetic variation of the 69-kb plasmid among AHPNS related strains has not been investigated. This study aimed to analyze genetic composition and diversity of the 69-kb plasmid in strains isolated from shrimps affected by AHPNS. Plasmids recovered from V. parahaemolyticus strain VPE61 which represented typical AHPNS pathogenicity, strain VP2HP which did not represent AHPNS pathogenicity but was isolated from AHPNS affected shrimp and other AHPNS V. parahaemolyticus isolates in Genbank were investigated. Protein coding genes of the 69-kb plasmid from the strain VPE61 were identical to that of AHPNS strain from Vietnam except the inverted complement 3.4-kb transposon covering pirA and pirB. The strain VP2HP possessed remarkable large 183-kb plasmid which shared similar protein coding genes to those of the 69-kb plasmid from strain VPE61. However, the 3.4-kb transposon covering pirA and pirB was absent from the 183-kb plasmid in strain VP2HP. A number of protein coding genes from the 183-kb plasmid were also detected in other AHPNS strains. In summary, this study identified a novel 183-kb plasmid that is related to AHPNS causing strains. Homologous recombination of the 69-kb AHPNS plasmid and other naturally occurring plasmids together with loss and gain of AHPNS virulence genes in V. parahaemolyticus were observed. The outcome of this research enables understanding of plasmid dynamics that possibly affect variable degrees of AHPNS pathogenicity.