Details of a Researcher - YOKOTA Shinichi

Papers - YOKOTA Shinichi

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犬及び人由来フルオロキノロン耐性大腸菌におけるプラスミド介在性キノロン耐性遺伝子oqxABの検出

佐藤豊孝, 横田伸一, 内田郁夫, 大久保寅彦, 石原加奈子, 岡林環樹, 藤井暢弘, 田村豊

感染症学雑誌 ( (一社)日本感染症学会 ) 85 ( 臨増 ) 191 - 191 2011.03

フルオロキノロン耐性肺炎球菌，インフルエンザ菌に対する各種キノロン系抗菌薬の活性比較

横田伸一, 大越康雄, 藤井暢弘

日本臨床微生物学雑誌 21 ( 1 ) 17 - 24 2011 [Refereed]

犬および人由来フルオロキノロン耐性大腸菌の性状比較

佐藤豊孝, 横田伸一, 岡林環樹, 石原加奈子, 藤井暢弘, 田村豊

感染症学雑誌 ( (一社)日本感染症学会 ) 84 ( 6 ) 821 - 822 2010.11

Acquisition of a Transposon Encoding Extended-Spectrum beta-Lactamase SHV-12 by Pseudomonas aeruginosa Isolates during the Clinical Course of a Burn Patient

Shuji Uemura, Shin-ichi Yokota, Hirotoshi Mizuno, Eiji Sakawaki, Keigo Sawamoto, Kunihiko Maekawa, Katsutoshi Tanno, Kazuhisa Mori, Yasufumi Asai, Nobuhiro Fujii

ANTIMICROBIAL AGENTS AND CHEMOTHERAPY ( AMER SOC MICROBIOLOGY ) 54 ( 9 ) 3956 - 3959 2010.09 [Refereed]

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Fosfomycin suppresses RS-virus-induced Streptococcus pneumoniae and Haemophilus influenzae adhesion to respiratory epithelial cells via the platelet-activating factor receptor

Shin-ichi Yokota, Tamaki Okabayashi, Yuko Yoto, Tsukasa Hori, Hiroyuki Tsutsumi, Nobuhiro Fujii

FEMS MICROBIOLOGY LETTERS ( WILEY-BLACKWELL ) 310 ( 1 ) 84 - 90 2010.09 [Refereed]

Human respiratory syncytial virus (RSV) sometimes causes acute and severe lower respiratory tract illness in infants and young children. The platelet-activating factor (PAF) receptor, which is a receptor for Streptococcus pneumoniae and Haemophilus influenzae, is upregulated by RSV infection in the pulmonary epithelial cell line A549. Fosfomycin, an antimicrobial agent, significantly suppressed PAF receptor induction by RSV infection at the mRNA and cell surface expression levels. Fosfomycin also suppressed RSV-induced adhesion of fluorescence-labeled S. pneumoniae and H. influenzae cells, as determined by flow cytometry and fluorescence microscopy. The RSV-induced bacterial adhesion was suggested to be host-PAF-receptor and bacterial-phosphocholine mediated. Fosfomycin, which has been shown to exhibit antimicrobial and immunomodulatory activities, was found here to suppress adhesion by disease-causing bacteria. Thus, fosfomycin might prevent secondary bacterial infection during RSV infection.

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犬由来フルオロキノロン-セファロスポリン多剤耐性大腸菌の系統発生分類による解析

佐藤豊孝, 横田伸一, 大久保寅彦, 石原加奈子, 岡林環樹, 藤井暢弘, 田村豊

日本獣医学会学術集会講演要旨集 ( (公社)日本獣医学会 ) 150回 253 - 253 2010.09

Increased Caspase-2 Activity is Associated with Induction of Apoptosis in IFN-beta Sensitive Melanoma Cell Lines

Takafumi Kamiya, Tamaki Okabayashi, Shin-ichi Yokota, Yuji Kan, Jiro Ogino, Toshiharu Yamashita, Nobuhiro Fujii, Kowichi Jimbow

JOURNAL OF INTERFERON AND CYTOKINE RESEARCH ( MARY ANN LIEBERT INC ) 30 ( 5 ) 349 - 357 2010.05 [Refereed]

Interferon (IFN) is believed to be one of the most effective anti-melanoma agents. Specifically, IFN-beta has the ability to induce apoptosis of melanoma cells. Induction of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has also been suggested to have a critical role in IFN-beta-induced apoptosis. To characterize the signaling pathway involved in IFN-beta-induced apoptosis, we analyzed the biological effects of IFN-beta on the cell death and caspase activation of melanoma cells. IFN-sensitive cell lines, MM418, SK-mel-23, and SK-mel-118, showed increased apoptotic populations correlated with the activation of caspase-2 and caspase-3 by IFN-beta. IFN-beta-induced apoptosis was significantly suppressed by inhibitors for caspase-2 or caspase-3, but not by inhibitors for caspase-8 or caspase-9 in these cell lines. TRAIL expression was observed in IFN-beta-treated cells of SK-mel-23 and SK-mel-118, but not in those cells of MM418, which showed massive IFN-beta-induced apoptosis and resistance to exogenous TRAIL-mediated apoptosis. G361 was resistant to IFN-beta-induced apoptosis but sensitive to exogenous TRAIL-mediated apoptosis. Furthermore, IFN-beta pretreatment significantly increased the sensitivity against exogenous TRAIL-mediated apoptosis and activation of caspase-2 in G361. These results suggested that caspase-2 activation is commonly associated with induction of IFN-beta-induced apoptosis in IFN-beta-sensitive melanoma cells.

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Pulmonary Collectins Protect Macrophages against Pore-forming Activity of Legionella pneumophila and Suppress Its Intracellular Growth

Kaku Sawada, Shigeru Ariki, Takashi Kojima, Atsushi Saito, Masami Yamazoe, Chiaki Nishitani, Takeyuki Shimizu, Motoko Takahashi, Hiroaki Mitsuzawa, Shin-ichi Yokota, Norimasa Sawada, Nobuhiro Fujii, Hiroki Takahashi, Yoshio Kuroki

JOURNAL OF BIOLOGICAL CHEMISTRY ( AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC ) 285 ( 11 ) 8434 - 8443 2010.03 [Refereed]

Pulmonary collectins, surfactant proteins A (SP-A) and D (SP-D), play important roles in innate immunity of the lung. Legionella pneumophila is a bacterial respiratory pathogen that can replicate within macrophages and causes opportunistic infections. L. pneumophila possesses cytolytic activity, resulting from insertion of pores in the macrophage membrane upon contact. We examined whether pulmonary collectins play protective roles against L. pneumophila infection. SP-A and SP-D bound to L. pneumophila and its lipopolysaccharide (LPS) and inhibited the bacterial growth in a Ca(2+)-dependent manner. The addition of LPS in the culture blocked the inhibitory effects on L. pneumophila growth by the collectins, indicating the importance of LPS-collectin interaction. When differentiated THP-1 cells were infected with L. pneumophila in the presence of SP-A and SP-D, the number of permeable cells was significantly decreased, indicating that pulmonary collectins inhibit pore-forming activity of L. pneumophila. The number of live bacteria within the macrophages on days 1-4 after infection was significantly decreased when infection was performed in the presence of pulmonary collectins. The phagocytosis experiments with the pH-sensitive dye-labeled bacteria revealed that pulmonary collectins promoted bacterial localization to an acidic compartment. In addition, SP-A and SP-D significantly increased the number of L. pneumophila co-localized with LAMP-1. These results indicate that pulmonary collectins protect macrophages against contact-dependent cytolytic activity of L. pneumophila and suppress intracellular growth of the phagocytosed bacteria. The promotion of lysosomal fusion with Legionella-containing phagosomes constitutes a likely mechanism of L. pneumophila growth suppression by the collectins.

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薬剤耐性北海道で分離されたキノロン耐性大腸菌臨床分離株の分子疫学的解析

横田伸一, 佐藤豊孝, 大越康雄, 岡林環樹, 田村豊, 藤井暢弘

感染症学雑誌 ( (一社)日本感染症学会 ) 84 ( 臨増 ) 226 - 227 2010.03

犬および人由来フルオロキノロン耐性大腸菌の性状比較

佐藤豊孝, 横田伸一, 岡林環樹, 石原加奈子, 藤井暢弘, 田村豊

感染症学雑誌 ( (一社)日本感染症学会 ) 84 ( 臨増 ) 436 - 436 2010.03

Cerebrospinal fluids containing anti-HSP70 autoantibodies from multiple sclerosis patients augment HSP70-induced proinflammatory cytokine production in monocytic cells

Shin-ichi Yokota, Susumu Chiba, Hiroyasu Furuyama, Nobuhiro Fujii

JOURNAL OF NEUROIMMUNOLOGY ( ELSEVIER SCIENCE BV ) 218 ( 1-2 ) 129 - 133 2010.01 [Refereed]

Anti-heat shock protein 70 (HSP70) autoantibodies are found in cerebrospinal fluids (CSF) from patients with multiple sclerosis. These autoantibodies cross-reacted not only with HSP70 and heat shock cognate protein 70 (HSC70). but also with a bacterial homologue, DnaK. CSF with a high anti-HSP70 autoantibody titer enhanced HSP70-induced proinflammatory cytokine and chemokine production in the human monocytic cell line, THP-1. Thus. anti-HSP70 autoantibodies in the CSF of multiple sclerosis patients may play a pathophysiological role in enhancing inflammation. (C) 2009 Elsevier B.V. All rights reserved.

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Helicobacter pylori Lipopolysaccharides Upregulate Toll-Like Receptor 4 Expression and Proliferation of Gastric Epithelial Cells via the MEK1/2-ERK1/2 Mitogen-Activated Protein Kinase Pathway

Shin-ichi Yokota, Tamaki Okabayashi, Michael Rehli, Nobuhiro Fujii, Ken-ichi Amano

INFECTION AND IMMUNITY ( AMER SOC MICROBIOLOGY ) 78 ( 1 ) 468 - 476 2010.01 [Refereed]

Helicobacter pylori is recognized as an etiological agent of gastroduodenal diseases. H. pylori produces various toxic substances, including lipopolysaccharide (LPS). However, H. pylori LPS exhibits extremely weakly endotoxic activity compared to the typical LPS, such as that produced by Escherichia coli, which acts through Toll-like receptor 4 (TLR4) to induce inflammatory molecules. The gastric epithelial cell lines MKN28 and MKN45 express TLR4 at very low levels, so they show very weak interleukin-8 (IL-8) production in response to E. coli LPS, but pretreatment with H. pylori LPS markedly enhanced IL-8 production induced by E. coli LPS by upregulating TLR4 via TLR2 and the MEK1/2-ERK1/2 pathway. The transcription factor NF-Y was activated by this signal and promoted transcription of the tlr4 gene. These MEK1/2-ERK1/2 signal-mediated activities were more potently activated by LPS carrying a weakly antigenic epitope, which is frequently found in gastric cancers, than by LPS carrying a highly antigenic epitope, which is associated with chronic gastritis. H. pylori LPS also augmented the proliferation rate of gastric epithelial cells via the MEK1/2-ERK1/2 pathway. H. pylori LPS may be a pathogenic factor causing gastric tumors by enhancing cell proliferation and inflammation via the MEK1/2-ERK1/2 mitogen-activated protein kinase cascade in gastric epithelial cells.

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Helicobacter pylori の主要な感染経路は母子感染である―random amplified polymorphic DNA fingerprinting法による検討―

今野武津子, 横田伸一, 藤井暢弘

日本ヘリコバクター学会誌 11 ( 2 ) 59 - 65 2010 [Invited]

Nrc of Streptococcus pneumoniae suppresses capsule expression and enhances anti-phagocytosis

Masaya Yamaguchi, Yuki Minamide, Yutaka Terao, Ryutaro Isoda, Taiji Ogawa, Shin-ichi Yokota, Shigeyuki Hamada, Shigetada Kawabata

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS ( ACADEMIC PRESS INC ELSEVIER SCIENCE ) 390 ( 1 ) 155 - 160 2009.12 [Refereed]

Streptococcus pneumoniae is a major pathogen of community-acquired pneumonia and one of its major virulence factors is pneumolysin, which functions as a cholesterol-dependent cytolytic pore-forming toxin. In this study, we identified the ply-like gene spd0729 in a BLAST search. Unexpectedly, hemolytic and cytotoxic assays showed no significant differences between a Delta spd0729 mutant strain and the wildtype strain, whereas the mutant strain exhibited weaker anti-phagocytic activity in human peripheral blood. In addition, real-time RT-PCR analysis revealed that four capsular biosynthesis genes in the mutant strain had expressions 7- to 432-fold greater than those of the wild type, while an enzyme-linked immunoassay showed a mean 3-fold greater amount of total capsular polysaccharide in the mutant strain. These results suggest that Spd0729 is not a cytolysin, though it plays crucial roles in anti-phagocytosis and regulation of capsule expression. Thus, we named Spd0729 as a negative regulator of capsular polysaccharide synthesis (Nrc). (c) 2009 Elsevier Inc. All rights reserved.

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Susceptibility and bactericidal activity of 8 oral quinolones against conventional-fluoroquinolone-resistant Streptococcus pneumoniae clinical isolates

Shin-ichi Yokota, Yasuo Ohkoshi, Nobuhiro Fujii

DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE ( ELSEVIER SCIENCE INC ) 65 ( 1 ) 76 - 80 2009.09 [Refereed]

We evaluated the pharmacokinetic/pharmacodynamic parameters of 8 oral quinolones (ciprofloxacin, garenoxacin [GRNX], gatifloxacin, levofloxacin, moxifloxacin, prulifloxacin, sitafloxacin, and sparfloxacin) on 11 fluoroquinolone-resistant Streptococcus pneumoniae strains, screened from 780 strains isolated from various clinical sources in Japan. GRNX showed the highest area under the blood concentration time curve/MIC ratios, which exceeded the target values for bacterial eradication against all fluoroquinolone-resistant S. pneumoniae strains. (C) 2009 Elsevier Inc. All rights reserved,

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High prevalence of beta-lactam-resistant Haemophilus influenzae type b isolates derived from respiratory tract specimens in Japanese patients

Shin-ichi Yokota, Yasuo Ohkoshi, Kiyoshi Sato, Nobuhiro Fujii

INTERNATIONAL JOURNAL OF INFECTIOUS DISEASES ( ELSEVIER SCI LTD ) 13 ( 5 ) 584 - 588 2009.09 [Refereed]

Objective: Serotypeable strains of Haemophilus influenzae, which can cause invasive infections, are found in the respiratory tract at low frequencies. We compared the antibiotic resistance of the typeable and nontypeable strains of H. influenzae in respiratory tract specimens obtained in Japan. Methods: We determined the serotypes and the antibiotic susceptibilities of 440 clinical H. influenzae strains isolated from respiratory tract specimens. We also examined the prevalence of genotypes that are associated with P-lactam resistance. Results: The majority of the strains were nontypeable (421 strains, 95.7%). The remainder belonged to serotypes b (10 strains, 2.3%), e (three strains, 0.7%), or f (six strains, 1.4%). The type b strains exhibited the expression of beta-lactamase and resistance mutations in penicillin-binding protein 3 with significantly higher frequencies than other strains. Conclusions: H. influenzae type b strains, which are associated with meningitis and bacteremia, derived from respiratory tract specimens, shared more p-lactam-resistant mechanisms than nontypeable and other serotype strains. (C) 2008 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.

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RSV replication is attenuated by counteracting expression of the suppressor of cytokine signaling (SOCS) molecules

Koichi Hashimoto, Kei Ishibashi, Ken Ishioka, Dongchi Zhao, Masatoki Sato, Shinichiro Ohara, Yusaku Abe, Yukihiko Kawasaki, Yuka Sato, Shin-ichi Yokota, Nobuhiro Fujii, Ray Stokes Peebles, Mitsuaki Hosoya, Tatsuo Suzutani

VIROLOGY ( ACADEMIC PRESS INC ELSEVIER SCIENCE ) 391 ( 2 ) 162 - 170 2009.09 [Refereed]

Human RSV causes an annual epidemic of respiratory tract illness in infants and in elderly. Mechanisms by which RSV antagonizes IFN-mediated antiviral responses include inhibition of type I IFN mRNA transcription and blocking signal transduction of JAK/STAT family members. The suppressor of cytokines signaling (SOCS) gene family utilizes a feedback loop to inhibit cytokine responses and block the activation of the JAK/STAT signaling pathway. To evaluate the potential of SOCS molecules to subvert the innate immune response to RSV infection, eight SOCS family genes were examined. RSV infection up-regulated SOCS1, SOCS3, and CIS mRNA expression in HEp-2 cells, Suppression of SOCS 1, SOCS3 and CIS by short interfering ribonucleic acid (siRNA) inhibited viral replication. Furthermore, inhibition of SOCS1, SOCS3, or CIS activated type I IFN signaling by inducing STAT1/2 phosphorylation. These results suggest that RSV infection escapes the innate antiviral response by inducing SOCS1, SOCS3 or CIS expression in epithelial cells. (C) 2009 Elsevier Inc. All rights reserved.

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Fosfomycin Suppresses Chemokine Induction in Airway Epithelial Cells Infected with Respiratory Syncytial Virus

Tamaki Okabayashi, Shin-ichi Yokota, Yuko Yoto, Hiroyuki Tsutsumi, Nobuhiro Fujii

CLINICAL AND VACCINE IMMUNOLOGY ( AMER SOC MICROBIOLOGY ) 16 ( 6 ) 859 - 865 2009.06 [Refereed]

Respiratory syncytial virus (RSV) infects airway epithelial cells, causing bronchiolitis and pneumonia. Inflammation is mediated by various cytokines secreted from RSV-infected airway epithelial cells, and it promotes the pathogenesis of RSV-related diseases. Fosfomycin (FOF) is approved as a treatment for various bacterial infectious diseases, including respiratory infectious diseases, in Japan. FOF is suggested to exhibit immunomodulatory effects on lipopolysaccharide-stimulated monocytes and T lymphocytes, in addition to its antimicrobial activity. We investigated the effect of FOF on the cytokine production of an airway epithelial cell line, A549, infected with RSV. RSV-induced cytokines, such as regulated on activation, normal T-cell expressed and secreted (RANTES), interleukin-8 (IL-8), and IL-6, in infected A549 cells. We found that FOF decreased the levels of RSV-induced RANTES and IL-8 but not the level of RSV-induced IL-6. The RANTES promoter was activated by RSV infection. Site-directed mutagenesis analysis of the RANTES promoter showed that NF-kappa B-binding motifs had a critical role in RSV-induced RANTES promoter activity. A luciferase reporter gene assay and a DNA-binding assay indicated that FOF suppressed the NF-kappa B activity induced by RSV infection. These results demonstrate that FOF treatment suppresses the RSV-induced transcription of the chemokines RANTES and IL-8 in airway epithelial cells.

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犬由来大腸菌のフルオロキノロン耐性機構

佐藤豊孝, 石原加奈子, 村松康和, 上野弘志, 岡林環樹, 横田伸一, 藤井暢弘, 田村豊

日本獣医学会学術集会講演要旨集 ( (公社)日本獣医学会 ) 146回 319 - 319 2008.09

Antibiotic susceptibility of Haemophilus influenzae strains isolated from various clinical sources in Hokkaido Prefecture, Japan

Yasuo Ohkoshi, Shin-Ichi Yokota, Kiyoshi Sato, Tasuku Hayashi, Keiko Matsuda, Osamu Kuwahara, Hirotsugu Akizawa, Nobuhiro Fujii

Journal of Infection and Chemotherapy ( Springer Japan ) 14 ( 2 ) 93 - 98 2008 [Refereed]

Any increase in β-lactam-resistant Haemophilus influenzae is a serious problem in respiratory and otolaryngology medicine. In this study, we examined the antibiotic susceptibility and genotype of 457 clinical Haemophilus influenzae strains isolated in Hokkaido Prefecture, Japan. Strains with β-lactam-resistant mutations in gene encoding penicillin-binding protein 3 were more frequently found in lower respiratory tract specimens (sputa) than in upper respiratory tract specimens, such as rhinorrhea. The existence of the TEM-1 β-lactamase gene occurred more frequently in adult patients than in pediatric patients. The results suggest that β-lactam-resistant or nonsusceptible strains are more prevalent in adult patients with respiratory diseases. We observed only a very few strains which were nonsuscpetible to third-generation cephalosporins (CEPs) and carbapenems. However, 12%-13% of the strains were shown to be resistant to penicillins and second-generation CEPs, and approximately 4% of the strains were shown to be nonsusceptible to fourth-generation CEPs. In addition, we identified tetracycline-resistant (2.8%), chloramphenicol-resistant (0.6%), clarithromycin-resistant (2.6%), and fluoroquinolone-nonsusceptible (approximately 2%) H. influenzae strains. © 2008 Japanese Society of Chemotherapy and The Japanese Association for Infectious Diseases.

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Papers - YOKOTA Shinichi