Faculty Profiles - YOKOTA Kenji

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Mucosal immunisation with Clostridium botulinum type C16Stoxoid and its non-toxic component

N Mahmut, K Inoue, Y Fujinaga, H Arimitsu, Y Sakaguchi, L Hughes, R Hirst, T Murphy, T Tsuji, T Watanabe, T Ohyama, T Karasawa, S Nakamura, K Yokota, K Oguma

JOURNAL OF MEDICAL MICROBIOLOGY 51 ( 10 ) 813 - 820 2002.10

Language：English Publisher：SOC GENERAL MICROBIOLOGY

Clostridium botulinum types C and D produce a 16 S (500 kDa) toxin that is formed by conjugation of neurotoxin with a non-toxic component (nonTox). The amino acid sequences of type C and D nonTox components are almost identical. In a previous report it was proposed that nonTox is necessary for the effective absorption of the toxin from the small intestine. This suggested the hypothesis that mucosal immunity against nonTox in the small intestine might prevent the absorption of both C- and D-16 S toxins. The nonTox was purified from a mutant strain, (C)-N71, that does not produce neurotoxin. This nonTox or detoxified C-16 S toxin were mixed with adjuvant (a mutant form of heat-labile toxin of Escherichia coli), and inoculated into mice via the nasal or oral route, or both. The mice inoculated nasally four times with nonTox or toxoid produced high levels of antibodies (including IgA) against the immunogens, both in intestinal fluids and sera. When these nonTox-immunised mice were challenged orally with 2 and 20 oral minimum lethal doses (MLD) of C- or D-16 S toxins, the same results were obtained with both C and D; the mice survived after challenge with 2 MLD of either C or D but were killed by 20 MLD of either toxin although the time to death was significantly longer than in the control non-immunised mice. These results indicate that the local anti-nonTox antibodies reduce absorption of both C- and D-16 S toxins from the small intestine. The C-16 S toxoid-immunised mice showed similar behaviour with type D toxin challenge, probably due to the same mechanism, but were protected against 20 MLD of C-16 S toxin.

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Randomized open trial for comparison of proton pump inhibitors in triple therapy for Helicobacter pylori infection in relation to CYP2C19 genotype

T Inaba, M Mizuno, K Kawai, K Yokota, K Oguma, M Miyoshi, S Take, H Okada, T Tsuji

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY 17 ( 7 ) 748 - 753 2002.7

Language：English Publisher：BLACKWELL PUBLISHING ASIA

Background and aims: Genetic polymorphism of cytochrome P450 (CYP) 2C19 influences the efficacy of Helicobacter pylori eradication therapy with a proton pump inhibitor (PPI) and amoxicillin. However, in triple therapy (PPI plus amoxicillin and clarithromycin), little is known about the impact of CYP2C19 polymorphism, or the use of rabeprazole, which is not well metabolized by CYP2C19. The efficacy of three PPI (omeprazole, lansoprazole, and rabeprazole) in a 1-week triple regimen were compared in relation to CYP2C19 polymorphism.
Method: One hundred and eighty-three patients were randomized to receive one of the following regimens: amoxicillin 500 mg t.i.d., clarithromycin 200 mg t.i.d., and PPI (omeprazole 20 mg, lansoprazole 30 mg, or rabeprazole 10 mg) b.i.d. CYP2C19 polymorphism was analyzed by PCR restriction fragment length polymorphism.
Results: Intention-to-treat-based overall cure rates for omeprazole, lansoprazole or rabeprazole regimens were 83.1% (95% confidence interval (CI): 69-89%), 86.7% (CI: 75-93%), and 76.6% (CI: 64-85%), respectively, without significant difference. The cure rate of the rabeprazole regimen (but not the lansoprazole or omeprazole regimens) tended to be correlated with CYP2C19 genotypes (P = 0.076). In patients with a homozygous extensive metabolizer genotype, the per protocol-based cure rate with rabeprazole (62.5%) was significantly lower than that with lansoprazole (90.0%; P = 0.038).
Conclusion: The overall cure rate of 1-week triple therapy for H. pylori eradication was not significantly different between regimens with omeprazole, lansoprazole or rabeprazole, but the impact of CYP2C19 genetic polymorphism on the cure rate appeared to differ between these PPI. (C) 2002 Blackwell Publishing Asia Pty Ltd.

DOI： 10.1046/j.1440-1746.2002.02790.x

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Reinfection rate following effective therapy against Helicobacter pylori infection in Japan

M Adachi, M Mizuno, K Yokota, M Miyoshi, Y Nagahara, T Maga, K Ishiki, T Inaba, H Okada, K Oguma, T Tsuji

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY 17 ( 1 ) 27 - 31 2002.1

Language：English Publisher：BLACKWELL PUBLISHING ASIA

Background and Aim: In developed countries, reinfection of Helicobacter pylori (H. pylori) after eradication of the bacterium is unusual, while the reinfection rate in developing countries is variable. In this study, we determined the reinfection rate after successful H. pylori eradication in Japan, a country with a high prevalence of H. pylori infection.
Methods: After successful eradication, 377 patients were followed up by endoscopy and urea breath test annually. In reinfected patients, H. pylori strains isolated initially and after reinfection were compared by using random amplification of polymorphic DNA fingerprinting.
Results: H. pylori became positive in four of 337 patients (1.2%) 1 year after eradication and in two of 133 patients (1.5%) 2 years after eradication. One patient experienced an ulcer relapse 2 years after eradication therapy. Random amplification of polymorphic DNA fingerprinting of the isolated strains from four of the six patients showed two had identical strains (at 1 year) while the other two had different strains (one at 1 year and one at 2 years). When infection in the two patients reinfected with identical strains is considered a recrudescence, the true reinfection rate is < 0.8% per patient year.
Conclusions: The reinfection rate after eradication of H. pylori is low in Japan despite the country's high prevalence of H. pylori infection. (C) 2002 Blackwell Science Asia Pty Ltd.

DOI： 10.1046/j.1440-1746.2002.02666.x

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臨床 H.pyloriのゲノムと病原性 (特集微生物ゲノム情報と医学--基礎と臨床)

林俊治, 平井義一, 横田憲治

現代医療 34 ( 5 ) 1091 - 1096 2002

Expression of heat shock protein 60 in normal and neoplastic human lymphoid tissues.

JIN Hua Shu, YOSHINO Tadashi, JIN Zaishun, OKA Takashi, KOBAYASHI Keita, YAMASAKI Rie, LIU Yi Xuan, YOKOTA Kenji, OGUMA Keiji, AKAGI Tadaatsu

J.Clin.Exp. Hematopathol 1, 25-32 ( 1 ) 25 - 32 2002

Language：English Publisher：The Japanese Society for Lymphoreticular Tissue Research

A molecular chaperonin in mammals, heat shock protein 60 (HSP60) is constitutively expressed in the mitochondria at a low level and is rapidly up-regulated under stress. However, the role of HSP60 in the lymphoid tissues has not been well clarified. In the present study, expression of HSP60 was examined by flow cytometry and immunohistochemistry in normal peripheral blood mononuclear cells, reactive lymphoid tissues, and malignant lymphomas. HSP60 was found to be present constitutively at low levels in a fraction of resting T cells and most monocytes. The blastic change upon mitogen stimulation induced HSP60 at much higher levels in more T, B and NK cells. In normal lymphoid tissues, HSP60 was expressed preferentially in the cytoplasm of large-sized lymphoid cells and macrophages in the germinal centers and the interfollicular area.<br>In non-Hodgkin lymphomas strong expression of HSP60 was detected in most cases of diffuse large B-cell lymphoma, follicular lymphoma, and grade 3 and NK/T cell lymphoma. No immunostaining was observed in low grade B-cell lymphomas, including follicular lymphoma, grade 1 and B-lymphoblastic lymphomas. HSP60 immunoreactivity was variable in T-cell lymphomas. Intense expression of HSP60 was observed in Reed-Sternberg cells in all cases of Hodgkin lymphoma.

DOI： 10.3960/jslrt.42.25

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Immunoglobulin G1 antibody response to Helicobacter pylori heat shock protein 60 is closely associated with low-grade gastric mucosa-associated lymphoid tissue lymphoma

E Ishii, K Yokota, T Sugiyama, Y Fujinaga, K Ayada, Hokari, I, S Hayashi, Y Hirai, M Asaka, K Oguma

CLINICAL AND DIAGNOSTIC LABORATORY IMMUNOLOGY 8 ( 6 ) 1056 - 1059 2001.11

Language：English Publisher：AMER SOC MICROBIOLOGY

Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is related to Helicobacter pylori infection. Specifically, it has been pointed out that pathogenesis of MALT lymphoma involves the 60-kDa heat shock protein (hsp60). To investigate humoral immune responses to the H. pylori hsp60 in patients with gastroduodenal diseases and patients with MALT lymphoma, the hsp60 of H. pylori was expressed with a glutathione S-transferase fusion protein and was purified (recombinant hsp60). Sera were obtained from H. pylori-positive patients with gastroduodenal diseases (MALT lymphoma, n = 13; gastric ulcer, n = 20; duodenal ulcer, n = 20; gastritis, n = 20) and from H. pylori-negative healthy volunteers (n = 9). Sera from patients with MALT lymphoma were also obtained at two times: before and after eradication therapy. Antibodies to hsp60 and H. pylori were assessed by enzyme-linked immunosorbent assay. The levels of immunoglobulin G (IgG) antibodies to the hsp60 of H. pylori-positive patients with gastroduodenal diseases were significantly elevated compared to those in the controls. The levels of IgG1 antibodies to hsp60 were elevated and correlated with the levels of anti-H. pylori antibodies in patients with MALT lymphoma. Humoral immunity against hsp60 may be important and relevant to gastroduodenal diseases induced by H. pylori infection.

DOI： 10.1128/CDLI.8.6.1056-1059.2001

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牛乳由来 globotriaosylceramide によるベロ毒素の細胞障害能の抑制

ターナ, 渡来仁, 児玉洋, 櫛泰典, 井上薫, 横田憲治, 小熊恵二

脂質生化学研究 43 203 - 206 2001.5

Inhibition of vero cell cytotoxic activity in Escherichia coli O157 : H7 lysates by globotriaosylceramide, Gb3, from bovine milk

S Watarai, Tana, K Inoue, Y Kushi, E Isogai, K Yokota, K Naka, K Oguma, H Kodama

BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY 65 ( 2 ) 414 - 419 2001.2

Language：English Publisher：TAYLOR & FRANCIS LTD

In order to clarify the presence and verotoxin (VT) inhibitory activity of globotriaosylceramide (Gb3) in bovine milk, we analyzed neutral glycosphingolipids (GSLs) from bovine milk and investigated the inhibitory effect of bovine milk Gb3 on the cytotoxicity of VT2. Five species of neutral GSLs, designated as N-1, N-2, N-3, N-4, and N-5, were separated on thin-layer chromatography (TLC). N-1, N-2, and N-3 showed the same mobility as glucosglceramide, lactosylceramide, and Gb3 on the TLC plate, respectively. N-4 and N-5 GSLs migrated below globoside on the TLC plate. N-3 GSL having the same TLC mobility as Gb3 from bovine milk was immunologically identified as Gb3 by monoclonal antibody against Gb3, anti-CD77 monoclonal antibody. Furthermore, the effect of bovine milk Gb3 on VT2-induced cytotoxicity mas investigated. We found that treatment of VT2 with bovine milk Gb3 can reduce the cytotoxic effect of VT2.

DOI： 10.1271/bbb.65.414

Relationship between susceptibility to hemolytic-uremic syndrome and levels of globotriaosylceramide in human sera

S Watarai, K Yokota, Tana, T Kishimoto, T Kanadani, K Taketa, K Oguma

JOURNAL OF CLINICAL MICROBIOLOGY 39 ( 2 ) 798 - 800 2001.2

Language：English Publisher：AMER SOC MICROBIOLOGY

The relationship between differential susceptibility to hemolytic-uremic syndrome (HUS) and levels of globotriaosylceramide (Gb3) in serum was studied in patients infected with verotoxin-producing Escherichia coli (VTEC). The serum Gb3 levels in patients with HUS were lower than these in diarrheal patients without subsequent HUS or in patients without clinical symptoms, indicating that individuals with a lower content of serum Gb3 show a higher incidence of HUS following VTEC infection.

DOI： 10.1128/JCM.39.2.798-800.2001

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H. pylori感染と胃粘膜免疫応答.

横田憲治, 綾田潔, 石井栄子, 山崎理恵, 小林計太, 吉野正, 林俊治, 平井義一, 赤木忠厚, 小熊恵二

日本臨床 59,342-348 2001

A randomized open trial for comparison of proton pump inhibitors, omeprazole versus rabeprazole, in dual therapy for Helicobacter pylori infection in relation to CYP2C19 genetic polymorphism

Masatsugu Miyoshi, Motowo Mizuno, Kuniharu Ishiki, Yasuhiro Nagahara, Toshirou Maga, Tomomi Torigoe, Junichirou Nasu, Hiroyuki Okada, Kenji Yokota, Keiji Oguma, Takao Tsuji

Journal of Gastroenterology and Hepatology (Australia) 16 ( 7 ) 723 - 728 2001

Language：English Publisher：Blackwell Publishing

Background and Aim: The genetic polymorphism of cytochrome P450 (CYP) 2C19 has been shown to influence the efficacy of Helicobacter pylori eradication therapy with a proton pump inhibitor (PPI) and amoxicillin (so-called dual therapy). Omeprazole, a widely used PPI, and rabeprazole, a new PPI, are metabolized in different pathways in terms of CYP2C19 genetic polymorphisms. In this study, we compared the efficacy of omeprazole and rabeprazole in a 2-week dual therapy in relation to CYP2C19 polymorphism. Methods: One hundred and ninety-nine patients with peptic ulcer disease were randomly assigned to receive one of the following regimens: 500 mg t.i.d. amoxicillin together with either 20 mg b.i.d. omeprazole or 10 mg b.i.d rabeprazole. The eradication of H. pylori was evaluated by using a bacterial culture and a [13C]-urea breath test at 1-2 months after completion of treatment. Cytochrome P4502C19 polymorphism was analyzed by using polymerase chain reaction-restriction fragment length polymorphism. Results: Intention-to-treat-based cure rates for the omeprazole or rabeprazole regimens were 66.3% (95% CI, 56-75) and 62.4% (95% CI, 52-71), respectively, without significant difference. Cytochrome P4502C19 genetic polymorphism did not influence the cure rates in either of these regimens. We analyzed various factors associated with treatment failure (PPI, CYP2C19 genotype, and smoking habit) by using multiple logistic regression
smoking was the only significant independent factor for treatment failure. Conclusion: Omeprazole and rabeprazole were equally effective in combination with amoxicillin in eradicating H. pylori, irrespective of the PPI used (omeprazole or rabeprazole) and CYP2C19 genetic polymorphism. Smoking significantly decreased the cure rate of H. pylori infection in the dual therapy. © 2001 Blackwell Science Asia Pty Ltd.

DOI： 10.1046/j.1440-1746.2001.02526.x

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Gastric mucosal immunity induced by H. pylori infection

K. Yokota, K. Ayada, E. Ishii, K. Oguma, R. Yamasaki, K. Kobayashi, T. Yoshino, T. Akagi, S. Hayashi, Y. Hirai

Nippon rinsho. Japanese journal of clinical medicine 59 ( 2 ) 342 - 348 2001

Language：Japanese Publishing type：Book review, literature introduction, etc.

H. pylori infection induces various humoral and cellular immunities in gastric mucosa. Some reports indicate predominant CD4+ cells infiltrate in H. pylori infected gastric mucosa, and these cells express the T helper 1 phenotype. Local humoral immunity is also induced. Gastric plasma cells produce anti-H. pylori antibodies, however, their protective immunity is not enough to eradicate bacteria in human. We found heat shock protein 60 kDa (hsp60) may be closely associated with pathogenesis in MALT lymphoma. IgG1 antibodies to hsp60 were significantly correlated with the antibodies to H. pylori whole cell in patients with MALT lymphoma. CD40-CD40L dependent B cell proliferation was induced by cytokine and/or hsp60 stimulations in those patients. Cytotoxicity of gastric epithelial cells which is associated with host immunity induced by H. pylori infection is still unclear. We found that lymphocytes from patients with peptic ulcer showed cytotoxicity to gastric cell line HGC-27 in vitro. Cytotoxicity was enhanced by cytokine stimulus to T-lymphocytes and by heat stress and/or patients' antibodies treatment of HGC-27 cells. The pathogenicity of H. pylori may involve not only bacterial virulence factor but also host immunity. Studies of mucosal local immunity will help explain the mechanisms of H. pylori induced gastrodoudenal diseases.

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CAP18(抗菌および抗エンドトキシン蛋白)の生体防御因子としての役割

平田陸正, 切替照雄, 横田憲治, 田村弘志, 田中重則, 小熊恵二, 佐藤成大

日本細菌学雑誌 55 ( 2 ) 347 2000.4

The Bacteriocidal Effect of the Electrolysed Functioning Water against Helicobacter pylori

NAKAO Miyuki, YOKOTA Kenji, OGUMA Keiji, TAKAI Kenichi

74 ( 2 ) 120 - 127 2000.2

H. pyloriの胃リンパ腫への関与

吉野正, 赤木忠厚, 横田憲治, 小熊恵二, 河原祥朗

癌の臨床 46:839-845 2000

Treatment of Helicobacter pylori infection

Hayashi, S, Hirai, Y, Isogai, H, Isogai, E, Yokota, K, Oguma, K

Res. Adv. Antimicrob. Chemother. 1 7 - 12 2000

Association of Helicobacter pylori with gastroduodenal diseases

Y Hirai, S Hayashi, H Shimomura, K Oguma, K Yokota

JAPANESE JOURNAL OF INFECTIOUS DISEASES 52 ( 5 ) 183 - 197 1999.10

Language：English Publishing type：Book review, literature introduction, etc. Publisher：NATL INST INFECTIOUS DISEASES

Helicobacter pylori was first cultured in vitro in 1982. This bacterium is a spiral gram negative rod which grows under microaerophilic conditions. The ecological niche is the mucosa of the human stomach which had been thought to be aseptic before the discovery of this bacterium. This organism causes a long-lasting infection throughout a person's life if there is no medical intervention. Numerous persons are infected with the organism around the world, and the rate of infection in Japan is nearly 50% of the population. However, the route of infection remains unclear because the organism has not been isolated from any environment other than several animals. H. pylori is now recognized as a causative agent of gastritis and peptic ulcers. Though gastritis, and especially chronic active gastritis, is observed at least histologically in all persons with H. pylori, peptic ulcers develop in only some infected persons. Specific factors in the host and/or the bacteria are needed for the development of peptic ulcer disease. Furthermore, H. pylori is considered to be related to the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma, especially those of low grade. Also, H. pylori infection is a major determinant for initiating the sequence of events leading to gastric cancer. In some patients with low-grade gastric MALT lymphoma, the eradication of H. pylori led to a regression of lesion. Gastric cancer has been induced in Mongolian gerbils with long-term H. pylori infection. The combinations of drugs, which consist of an antisecretory agent (acid-supressing agent) and antimicrobial agents, are used for the eradication of the organism. Eradication therapy is recommended at least for patients with peptic ulcers.

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Antibodies to human gastric epithelial cells and heat shock protein 60 in Helicobacter pylori positive mucosa associated lymphoid tissue lymphoma

Y Kawahara, K Yokota, M Mizuno, N Yunoki, T Uesu, H Okada, K Kobayashi, Y Hirai, K Oguma, T Tsuji

GUT 45 ( 1 ) 20 - 23 1999.7

Language：English Publisher：BRITISH MED JOURNAL PUBL GROUP

Background-Development of gastric mucosa associated lymphoid tissue (MALT) lymphoma is thought to be closely associated with host immune reactions to Helicobacter pylori.
Aim-To investigate humoral immune responses in patients with MALT lymphoma to antigens shared by PI pylori and human gastric epithelial cells. IC
Methods-Sera were obtained from H pylori positive patients with MALT lymphoma (n = 11) or other gastroduodenal diseases (peptic ulcer, n = 40; nonulcer dyspepsia, n = 20) and from H pylori, negative healthy control subjects (n = 10). Antibodies to HGC-27 human gastric epithelial cells and human recombinant heat shock protein (Hsp) 60 were examined using an enzyme linked immunosorbent assay (ELISA) and immunoblotting.
Results-Antibody titres to HGC-27 cells were significantly elevated in H pylori positive patients with MALT lymphoma when compared with titres in patients with other gastroduodenal diseases and in healthy subjects. Immunoblotting of sera from patients with MALT lymphoma often detected a band with a molecular mass corresponding to Hsp60, and both ELISA and immunoblotting showed elevated antibody titres to the recombinant human Hsp60. Antigenic similarity between Hsp60 and H pylori HspB was documented by immunoblotting experiments.
Conclusions-Autoantibodies reactive with host gastric epithelial cells are often increased in MALT lymphoma, and Hsp60 is a major target antigen. Immune responses induced by immunological cross reactivity between H pylori HspB and human Hsp60 in gastric epithelium may be involved in the development of MALT lymphoma.

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【感染症とその治療細菌感染症】ボツリヌス症

小熊惠二, 藤永由佳子, 井上薫, 横田憲治, 武士甲一

最新医学 54 ( 増刊 ) 652 - 664 1999.3

ボツリヌスprogenitor toxinのHAサブコンポーネントの小腸微絨毛及び赤血球への結合活性について

藤永由佳子, 井上薫, 横田憲治, 長町榮子, 小熊惠二

日本細菌学雑誌 54 ( 1 ) 117 - 117 1999.2

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