研究者詳細 - 横田　憲治

論文 - 横田　憲治

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Detection of Helicobacter hepaticus in Human Bile Samples of Patients with Biliary Disease 査読

Toshihide Hamada, Kenji Yokota, Kiyoshi Ayada, Kazuyuki Hirai, Tomoari Kamada, Ken Haruma, Kazuaki Chayama, Keiji Oguma

HELICOBACTER 14 ( 6 ) 545 - 551 2009年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：WILEY-BLACKWELL

Background: Since the discovery of Helicobacter pylori, various enterohepatic Helicobacter spices have been detected in the guts of humans and animals. Some enterohepatic Helicobacters have been associated with inflammatory bowel disease or liver disease in mice. However the association of these bacteria with human diseases remains unknown. Materials and
Methods: We collected 126 bile samples from patients with cholelithiasis, cholecystitis, gallbladder polyp, and other nonbiliary diseases. Samples were screened for the presence of enterohepatic Helicobacter spp. using Cultures, nested PCR, or in situ hybridization. We tested for antibodies to H. pylori and H. hepaticus by Western blot analysis.
Results: Attempts at cultivation were unsuccessful. However, H. hepaticus was detected in bile samples with nested PCR whereas H. bilis was not. Helicobacter hepaticus in the bile was confirmed by in situ hybridization, but H. hepaticus from bile samples was coccoid in appearance. We detected immunoglobulin G antibodies to H. hepaticus in bile samples by Western blotting. Helicobacter hepaticus was detected in 40 (32%) of total 126 samples as H. hepaticus positive if at least one of the three methods with nested PCR, in situ, or Western blotting. Patients with cholelithiasis (41%) and cholecystitis with gastric cancer (36%) had significantly higher (p = .029) prevalence of H. hepaticus infection than samples from patients with other diseases.
Conclusion: Helicobacter hepaticus may closely associate with diseases of the liver and biliary tract in humans.

DOI： 10.1111/j.1523-5378.2009.00729.x

Regulation of cellular immunity prevents Helicobacter pylori-induced atherosclerosis 査読

K. Ayada, K. Yokota, K. Hirai, K. Fujimoto, K. Kobayashi, H. Ogawa, K. Hatanaka, S. Hirohata, T. Yoshino, Y. Shoenfeld, E. Matsuura, K. Oguma

LUPUS 18 ( 13 ) 1154 - 1168 2009年11月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：SAGE PUBLICATIONS LTD

Helicobacter pylori (H. pylori) is a predominant pathogen that causes not only gastroduodenal diseases but also extra-alimentary tract diseases. In this study, we demonstrated that H. pylori infection promoted atherogenesis in heterozygous apoe(+/-) ldlr(+/-) mice. The male mice were fed with high fat diet from the age of 6 weeks. At the age of 16 weeks, development of atherosclerotic lesions was observed in the H. pylori-infected mice, and it seemed to be associated with an elevation of Th1-immune response against H. pylori origin-heat shock protein 60 (Hp-HSP60) and an increment of transendothelial migration of T cells. Subcutaneous immunisation with Hp-HSP60 or H. pylori eradication with antibiotics significantly reduced the progression of atherosclerosis, accompanied by a decline of Th1 differentiation and reduction of their chemotaxis beyond the endothelium. Thus, oral infection with H. pylori accelerates atherosclerosis in mice and the active immunisation with Hp-HSP60 or the eradication of H. pylori with antibiotics can moderate/prevent cellular immunity, resulting in a reduction of atherosclerosis. Lupus (2009) 18, 1154-1168.

DOI： 10.1177/0961203309106600

Anabolic utilization of steroid hormones in Helicobacter pylori 査読

Kouichi Hosoda, Hirofumi Shimomura, Shunji Hayashi, Kenji Yokota, Keiji Oguma, Yoshikazu Hirai

FEMS MICROBIOLOGY LETTERS 297 ( 2 ) 173 - 179 2009年8月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：WILEY-BLACKWELL PUBLISHING, INC

In this study, we have demonstrated that Helicobacter pylori absorbs a steroid prehormone (pregnenolone) and two androgens (dehydroepiandrosterone and epiandrosterone), glucosylates these steroids, and utilizes glucosyl-steroid hormone compounds as the membrane lipid components. The only common structure among the steroid prehormone and the two androgens is a 3 beta-OH in the steroid framework. Our results indicate that the 3 beta-OH in the steroid hormones is a crucial conformation required for steroid glucosylation by H. pylori. In addition, we found that H. pylori absorbs and holds estrogens possessing 3-OH (estrone and estradiol) into the membrane. The effective absorption of estrogen into the membrane appeared to be controlled by the number of hydroxyl groups modifying the steroid framework. In contrast, H. pylori induced neither membrane absorption nor glucosylation of the other steroid hormones possessing 3=O (progesterone, androstenedione and testosterone) or 3 alpha-OH (androsterone). These results indicate that H. pylori selectively absorbs 3 beta-OH and 3-OH steroid hormones, and utilizes only 3 beta-OH steroid hormones as the materials for glucosylation.

DOI： 10.1111/j.1574-6968.2009.01685.x

Chronic Infections and Atherosclerosis 査読

Kiyoshi Ayada, Kenji Yokota, Kazuko Kobayashi, Yehuda Shoenfeld, Eiji Matsuura, Keiji Oguma

CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY 37 ( 1 ) 44 - 48 2009年8月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：HUMANA PRESS INC

The immune response against heat shock protein 60 (HSP60) derived from pathogens causing chronic infections is thought to be an important pro-atherogenic mechanism because high serum levels of antibodies against HSP60 have been associated with atherosclerotic diseases, such as coronary artery diseases, or cerebro-vascular events. Furthermore, the presence of HSP60-specific T lymphocytes in circulation may increase the risk of atherosclerosis. Our recent in vitro and in vivo studies have also shown an association of Helicobacter pylori-HSP60 (Hp-HSP60) specific Th1 immune responses elicited by H. pylori infection with the progression of atherosclerosis in a hyperlipidemic mouse model. These Th1 dominant immune responses may cross-react with endogenous HSP60 expressed on stressed cells of the vascular endothelium, likely due to molecular mimicry. However, the exact mechanisms by which endothelial cells display their HSP60 molecule or present HSP60 antigenic epitopes on the surface are still unclear.

DOI： 10.1007/s12016-008-8097-7

Helicobacter pylori eradication may induce de novo, but transient and mild, reflux esophagitis: Prospective endoscopic evaluation 査読

Susumu Take, Motowo Mizuno, Kuniharu Ishiki, Yasuhiro Nagahara, Tomowo Yoshida, Kenji Yokota, Keij Oguma, Hiroyuki Okada, Kazuhide Yamamoto

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY 24 ( 1 ) 107 - 113 2009年1月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：WILEY-BLACKWELL PUBLISHING, INC

Backgrounds and Aim: The effect on reflux esophagitis of eradicating Helicobacter pylori is variable and not fully defined. We previously reported that in patients who have reflux esophagitis associated with duodenal ulcer, a significant improvement in the preexisting reflux esophagitis occurred after H. pylori was eradicated. In the present study, we asked whether H. pylori eradication leads to de novo development of reflux esophagitis in peptic ulcer patients.
Methods: Prospective post-eradication evaluations were conducted in 1195 H. pylori-positive patients with peptic ulcer diseases who were confirmed not to have reflux esophagitis by endoscopic examination before eradication therapy. After eradication therapy, endoscopy and a urea breath test were performed yearly.
Results: A total of 1187 patients were followed for up to 10.0 years (a mean of 3.6 years). Reflux esophagitis developed in 279 of 1000 patients cured of infection and in 26 of 187 patients who had persistent infection (P < 0.0001, Fisher's exact test). The esophagitis was mild (Los Angeles grade A) in most patients, transient in approximately one-half, and rarely necessitated long-term medication for the condition. Cure of infection, alcohol consumption, younger age, and high body mass index were identified as significant factors for the risk of developing non-transient reflux esophagitis.
Conclusions: Cure of H. pylori infection may increase the risk of developing reflux esophagitis in patients with peptic ulcer, but the esophagitis is mostly mild and transient, and long-term medication is rarely required. Thus, H. pylori eradication therapy need not be withheld for fear of provoking reflux esophagitis.

DOI： 10.1111/j.1440-1746.2008.05606.x

Helicobacter pylori heat shock protein 60 antibodies are associated with gastric cancer 査読

Aki Tanaka, Tomoari Kamada, Kenji Yokota, Akiko Shiotani, Jiro Hata, Keiji Oguma, Ken Haruma

PATHOLOGY RESEARCH AND PRACTICE 205 ( 10 ) 690 - 694 2009年

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：ELSEVIER GMBH, URBAN & FISCHER VERLAG

Helicobacter pylori infection causes atrophic gastritis, peptic ulcer, and gastric cancer. The host immune response plays an important role in the pathogenesis of H. pylori-related diseases. Heat shock proteins are antigens involved in various diseases This study evaluated seropositivity for antibodies to H. pylori heat shock protein 60 in patients with gastric cancer.
Serum samples were obtained from 57 patients with gastric cancer (25 patients with diffuse-type gastric cancer and 32 with intestinal-type gastric cancer), 45 H. pylori-positive patients, and 49 H. pylori-negative patients without gastric cancer. Antibodies to heat shock protein 60 and H. pylori were assessed by enzyme-linked immunosorbent assay.
The positivity rate for antibodies to hsp60 was significantly higher in H pylori-positive patients than in H. pylori-negative patients (73.3% vs. 24.5%. p<0.001). In addition, the positivity rate for antibodies to hsp60 was higher in patients with gastric cancer than in H. pylori-positive patients without gastric cancer (87.7% vs. 73.3%, p = 0.06), and the positivity rate for antibodies to hsp60 was significantly higher in patients with diffuse-type gastric cancer than in M pylori-positive patients Without gastric cancer (96% vs. 73 3%, p<0.05).
H. pylori hsp60 might be associated with gastric carcinogenesis, especially in the case of diffuse cancer. (C) 2009 Elsevier GmbH. All rights reserved.

DOI： 10.1016/j.prp.2009.04.008

Immune Reactions Against Elongation Factor 2 Kinase: Specific Pathogenesis of Gastric Ulcer from Helicobacter pylori Infection 査読

Kiyoshi Ayada, Kenji Yokota, Yoshiro Kawahara, Yumiko Yamamoto, Kazuyuki Hirai, Tomoki Inaba, Masahide Kita, Hiroyuki Okada, Kazuhide Yamamoto, Keiji Oguma

CLINICAL & DEVELOPMENTAL IMMUNOLOGY 2009年

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：HINDAWI PUBLISHING CORPORATION

Helicobacter pylori (H. pylori) infection is a definite causative factor for gastric ulcers (GUs). In the present study we detected a specific antigen of gastric epithelial cells (HGC-27) using cell ELISA, which was recognized by the sera of GU patients (n = 20) but not in patients with chronic gastritis (CG; n = 20) or in healthy volunteers (HC; n = 10). This antigen was over-expressed by a stressful (heat-stressed) environment, and was identified as elongation factor 2 kinase (EF-2K) by western blotting. The GU patients' lymphocytes stimulated by H. pylori specifically disrupted heat-stressed HGC-27 cells in a cytotoxic assay. In flow cytometry, the effector cells (lymphocytes) from GU patients were significantly differentiated to T helper type 1 lymphocyte (Th1) and cytotoxic T lymphocyte (CTL) as opposed to those from CG patients. The target cells (HGC-27) expressed EF-2K and MHC-class I together with costimulatory molecules from heat stress. This antigen specific immune mechanism could have a prominent role in the pathogenesis of GU. Copyright (C) 2009 Kiyoshi Ayada et al.

DOI： 10.1155/2009/850623

The role of streptococcal hypersensitivity in the pathogenesis of Behçet's Disease. 査読

Kaneko F, Oyama N, Yanagihori H, Isogai E, Yokota K, Oguma K

European journal of dermatology : EJD 18 ( 5 ) 489 - 498 2008年9月

Antibodies against heat shock protein 60 derived from Helicobacter pylori: Diagnostic implications in cardiovascular disease

Tomoyuki Okada, Kiyoshi Ayada, Shinichi Usui, Kenji Yokota, Jinhua Cui, Yoshiro Kawahara, Tomoki Inaba, Satoshi Hirohata, Motowo Mizuno, Daisuke Yamamoto, Shozo Kusachi, Eiji Matsuura, Keiji Oguma

Journal of Autoimmunity 29 ( 2-3 ) 106 - 115 2007年9月

掲載種別：研究論文（学術雑誌）

Immune responses against heat shock protein 60 (HSP60) of pathogen-origin are thought to be defensive events which, due to molecular mimicry, misdirect to a human counterpart. Therefore, atherosclerosis may be serologically predicted by anti-HSP60 antibodies (Abs). In the present study, we analyzed the clinical prevalence of the serum IgG Abs against Helicobacter pylori (Hp)-derived HSP60 (Hp-HSP60) or its peptide fragments in patients with cardiovascular disease (CVD; n = 250), as compared to those in age- and gender-matched non-CVD patients (n = 293). Anti-Hp cell lysate Abs frequently appeared in Hp-infected patients who were not associated with CVD. In contrast, Abs against the particular amino acid sequence Hp-HSP60II3 (II3 region, Glu141-Leu160, in Hp-HSP60) predominantly appeared in CVD patients, as well as IgG anti-human HSP60 (Hu-HSP60w). Furthermore, neither titer of anti-Hp-HSP60II3 nor anti-Hu-HSP60w Abs was correlated with the levels of high sensitivity C-reactive protein (hsCRP). This data strongly suggested that IgG anti-Hp-HSP60II3 Abs cross-reacted with Hu-HSP60w were independent diagnostic markers relevant to CVD. Further, the 20 amino acid residues (Glu141-Leu160) might be predominant CVD-associated epitopes that induce anti-Hu-HSP60 auto-Abs, whose location was predicted in the tertiary structure of Hu-HSP60. © 2007 Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.jaut.2007.05.004

Conversion of flavodoxin from holoenzyme to apoprotein during growth phase changes in Helicobacter pylori 査読

Hirofumi Shimomura, Shunji Hayashi, Kenji Yokota, Keiji Oguma, Yoshikazu Hirai

JOURNAL OF BACTERIOLOGY 189 ( 13 ) 4960 - 4963 2007年7月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：AMER SOC MICROBIOLOGY

The catabolic pathway for flavodoxin has yet to be clarified for any bacterial species. In this study, we found that the flavin mononucleotide in the flavodoxin of Helicobacter pylori is degraded to riboflavin via the phosphomonoesterase activity of class C acid phosphatase. The result is a conversion of holoflavodoxin to apoflavodoxin.

DOI： 10.1128/JB.00272-07

Helicobacter pylori heat-shock protein 60 induces interleukin-8 via a Toll-like receptor (TLR)2 and mitogen-activated protein (MAP) kinase pathway in human monocytes 査読

Ying Zhao, Kenji Yokota, Kiyoshi Ayada, Yumiko Yamamoto, Tomayuki Okada, Lianhua Shen, Keiji Oguma

JOURNAL OF MEDICAL MICROBIOLOGY 56 ( 2 ) 154 - 164 2007年2月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：SOC GENERAL MICROBIOLOGY

Previous reports have indicated that Helicobacter pylori heat-shock protein 60 (H. pylori-HSP60), as an immunodominant antigen, induces interleukin (IL)-8 production in human monocytes. The exact mechanism by which H. pylori-HSP60 induces IL-8 production in monocytes has not been fully elucidated. In the present study, the downstream pathway by which H. pylori-HSP60 induces IL-8 secretion in human monocytic cell lines was investigated. Intact H. pylori, heat-killed H. pylori and H. pylori recombinant HSP60 (rHpHSP60) all induced the secretion of IL-8 and the activation of mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK) and p38, but not c-Jun N-terminal kinase (JNK), up to 24 In in NOMO1 cells. The specific inhibitors PD98059 and U0126 (for ERK1/2 signalling) and SB203580 (for p38 MAPK signalling) down-regulated IL-8 secretion from rHpHSP60-treated NOMO1 cells. An anti-Toll-like receptor (TLR)2 antibody or TLR2 small interfering RNA (siRNA) partialiy inhibited the secretion of IL-8, and anti-TLR2 antibody also suppressed activation of ERK and p38 MAPK in rHpHSP60-treated NOMO1 cells. These reactions were associated with nuclear factor-kappa B (NF-kappa B)-mediated transcriptional activation, since U01 26, SB203580 and the anti-TLR2 antibody decreased NF-kappa B activation. Taken together, the results suggest that ERK and p38 MAPK signalling linked to the TLR2 recognition receptor in human monocytes may be an important pathway in H. pylori-HSP60-induced IL-8 secretion.

DOI： 10.1099/jmm.0.46882-0

Baseline gastric mucosal atrophy is a risk factor associated with the development of gastric cancer after Helicobacter pylori eradication therapy in patients with peptic ulcer diseases 査読

Susumu Take, Motowo Mizuno, Kuniharu Ishiki, Yasuhiro Nagahara, Tomowo Yoshida, Kenji Yokota, Keiji Oguma

JOURNAL OF GASTROENTEROLOGY 42 21 - 27 2007年1月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：SPRINGER TOKYO

Background. We previously reported that eradication of Helicobacter pylori could reduce the risk of developing gastric cancer in patients with peptic ulcer diseases. In the present study, we further followed up out-patient groups to identify factors associated with the development of gastric cancer. Methods. Prospective posteradication evaluations were conducted in 1342 consecutive patients (1191 men and 151 women; mean age, 50 years) with peptic ulcer disease who had received H. pylori eradication therapy. The patients had undergone endoscopic examination before eradication therapy to evaluate peptic ulcers, background gastric mucosa, and H. pylori infection. After confirmation of eradication, follow-up endoscopy was performed yearly. Results. A total of 1131 patients were followed for up to 9.5 years (mean, 3.9 years). Gastric cancer developed in 9 of 953 patients cured of infection and in 4 of 178 who had persistent infection (P = 0.04). The risk of developing gastric cancer after receiving H. pylori eradication therapy was increased according to the grade of baseline gastric mucosal atrophy (P = 0.01). In patients with peptic ulcer diseases, persistent infection of H. pylori (hazard ratio, 3.9; P = 0.03), the grade of baseline gastric mucosal atrophy (3.3, P = 0.01) and age (2.0, P = 0.04) were identified as significant risk factors for developing gastric cancer. Conclusions. The grade of gastric atrophy was closely related to the development of gastric cancer after receiving H. pylori eradication therapy. Thus, eradication of H. pylori before the significant expansion of atrophy is most beneficial to prevent gastric cancer.

DOI： 10.1007/s00535-006-1924-9

A better cure rate with 800 mg than with 400 mg clarithromycin regimens in one-week triple therapy for Helicobacter pylori infection in cigarette-smoking peptic ulcer patients 査読

Hidehiko Ishioka, Motowo Mizuno, Susumu Take, Kuniharu Ishiki, Yasuhiro Nagahara, Tomowo Yoshida, Hiroyuki Okada, Kenji Yokota, Keiji Oguma

DIGESTION 75 ( 2-3 ) 63 - 68 2007年

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：KARGER

Background/Aims: In Helicobacter pylori eradication therapy, using a proton pump inhibitor plus amoxicillin and clarithromycin (PPI/AC regimen), the impact of the clarithromycin dose and smoking on efficacy is conflicting. Here, we compared the efficacy of 400 and 800 mg of clarithromycin in the regimen in relation to smoking in patients with peptic ulcer disease. Methods: We studied 601H. pylori-positive patients with peptic ulcer disease who had received amoxicillin 750 mg and clarithromycin 200 or 400 mg together with lansoprazole 30 mg b. i. d. Results: 305 patients were treated with a regimen containing 400 mg of clarithromycin (C400 group), and 296 patients with a regimen containing 800 mg (C800 group). Overall cure rates between the two groups were not significantly different, but the cure rate in the C800 group was significantly better than that in the C400 group among patients infected with clarithromycin- sensitive strains (p = 0.03). This difference could be attributed to differences among smokers versus non-smokers: the cure rate among smokers in the C800 group (91.0%) was better than that in the C400 group (80.0%, p = 0.003). Conclusions: 800 mg of clarithromycin is recommended in the PPI/AC regimen for patients who smoke and are infected with clarithromycinsensitive H. pylori.

DOI： 10.1159/000102301

Chronic infections and atherosclerosis

Kiyoshi Ayada, Kenji Yokota, Kazuko Kobayashi, Yehuda Shoenfeld, Eiji Matsuura, Keiji Oguma

Annals of the New York Academy of Sciences 1108 594 - 602 2007年

記述言語：英語掲載種別：研究論文（国際会議プロシーディングス）出版者・発行元：Blackwell Publishing Inc.

Immunoinflammatory processes due to chronic infection are thought to be one of the definitive atherogenetic processes. Especially, anti-heat shock protein antibodies have been related to the prevalence of disease such as coronary artery disease or cerebral infarction, etc., resulted from atherosclerosis. Furthermore, the presence of HSP60-specific T lymphocytes in circulation may increase the risk of atherosclerosis. We have recently demonstrated the evidences that Helicobacter pylori infection induced atherosclerosis in apoe+/-ldlr+/- mice and that Hp-anti-heat-shock protein specific Th1-dominant immune responses had a major involvement in the progression of atherosclerosis. These cellular immune responses caused autoimmunity against endogenous HSP60 (expressed on the stressed cells of vascular endothelium), due to the molecular mimicry. Therefore, an appropriate treatment with antibiotics or with anti-HSP60 antibodies, which regulates the Th1 induction, could sufficiently reduce the progression of atherosclerosis. © 2007 New York Academy of Sciences.

DOI： 10.1196/annals.1422.062

Production of anti-neurotoxin antibody is enhanced by two subcomponents, HA1 and HA3b, of Clostridium botulinum type B 16S toxin–haemagglutinin 査読

Jae-Chul Lee, Kenji Yokota, Hideyuki Arimitsu, Hyun-Jung Hwang, Yoshihiko Sakaguchi, Jinhua Cui, Kouichi Takeshi, Toshihiro Watanabe, Tohru Ohyama, Keiji Oguma

Microbiology 151 ( 11 ) 3739 - 3747 2005年11月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Microbiology Society

<italic>Clostridium botulinum</italic> type B strain produces two forms of progenitor toxin, 16S and 12S. The 12S toxin is formed by association of a neurotoxin (NTX) and a non-toxic non-haemagglutinin (NTNH), and the 16S toxin is formed by conjugation of the 12S toxin with a haemagglutinin (HA). HA consists of four subcomponents designated HA1, HA2, HA3a and HA3b. When mice were immunized with formalin-detoxified NTX, 12S or 16S, a significantly greater amount of anti-NTX antibody (Ab) was produced in the mice injected with 16S than in NTX- or 12S-injected mice. Immunization with NTX mixed with HA1 and/or HA3b also increased the anti-NTX Ab production, whereas NTX mixed with HA2 did not, indicating that HA1 and HA3b have adjuvant activity. This was further confirmed by immunizing mice with human albumin (Alb) alone or Alb mixed with either HA1 or HA3b. When mouse-spleen cells were stimulated with NTX, 16S or different HA subcomponents, 16S, HA1, HA3b and the mixture of HA1 and HA3 significantly increased interleukin 6 (IL6) production compared with NTX alone. Transcription of IL6 mRNA was low after stimulation with NTX alone, but increased to 16S-stimulation levels when NTX was mixed with HA1 or HA3b. In flow cytometry using labelled Abs against CD3 and CD19, the percentage of CD19 cells was higher following stimulation with 16S or NTX mixed with HA1 or HA3b compared with stimulation with NTX. The percentage of CD3 cells remained unchanged. These results suggest strongly that HA1 and HA3b demonstrate adjuvant activity via increasing IL6 production.

DOI： 10.1099/mic.0.28421-0

HLA-DQA1*0103-DQB1*0601 haplotype and Helicobacter pylori-positive gastric mucosa-associated lymphoid tissue lymphoma 査読

Yoshiro Kawahara, Motowo Mizuno, Tadashi Yoshino, Kenji Yokota, Keiji Oguma, Hiroyuki Okada, Shigeatsu Fujiki, Yasushi Shiratori

Clinical Gastroenterology and Hepatology 3 ( 9 ) 865 - 868 2005年9月

記述言語：英語掲載種別：研究論文（学術雑誌）

Background &amp
Aims: Immune responses to Helicobacter pylori are important in the pathogenesis of gastric mucosa-associated lymphoid tissue (MALT) lymphoma. In this retrospective case study, we investigated whether certain alleles and haplotypes of major histocompatibility complex genes are associated with gastric MALT lymphoma and the efficacy of H pylori eradication therapy on the lymphoma. Methods: Blood samples were obtained from 18 patients with H pylori-positive gastric MALT lymphoma (5 men and 13 women
age range, 51-80 years), 30 patients with H pylori-positive non-ulcer dyspepsia (17 men and 13 women
age range, 37-77 years), and 30 patients with H pylori-negative non-ulcer dyspepsia (12 men and 18 women
age range, 37-77 years). HLA-DQA1 and DQB1 allele typing was performed by use of a polymerase chain reaction sequence-specific oligonucleotide procedure. All patients with MALT lymphoma were treated with H pylori eradication therapy and followed up by repeated endoscopy and biopsy. Results: We found a significant increase in alleles HLA-DQA1*0103 and HLA-DQB1*0601, and a haplotype DQA1*0103-DQB1*0601, in MALT lymphoma patients when compared with non-ulcer dyspepsia patients who were either H pylori-positive or not and with a healthy control population. After H pylori eradication, the lymphomas regressed completely in all 10 patients who possessed the DQA1*0103-DQB1*0601 haplotype but in only 4 of the 8 without this haplotype (P = .023). Conclusions: DQA1*0103-DQB1*0601 haplotype-positive gastric MALT lymphoma is likely to respond to therapy by eradication of H pylori. © 2005 by the American Gastroenterological Association.

DOI： 10.1016/S1542-3565(05)00185-0

The effect of eradicating Helicobacter pylori on the development of gastric cancer in patients with peptic ulcer disease 査読

Susumu Take, Motowo Mizuno, Kuniharu Ishiki, Yasuhiro Nagahara, Tomowo Yoshida, Kenji Yokota, Keiji Oguma, Hiroyuki Okada, Yasushi Shiratori

American Journal of Gastroenterology 100 ( 5 ) 1037 - 1042 2005年5月

記述言語：英語掲載種別：研究論文（学術雑誌）

OBJECTIVES: Infection with Helicobacter pylori is a risk factor for the development of gastric cancer. However, it is not known whether eradication therapy can prevent the development of gastric cancer in persons in whom the cancer is not yet established. In the present study, we investigated whether the eradication of H. pylori in patients with peptic ulcer disease reduces the likelihood of their developing gastric cancer. METHODS: Prospective posteradication evaluations were conducted in 1,342 consecutive patients (1,191 men and 151 women
mean age: 50 yr) with peptic ulcer diseases who had received H. pylori eradication therapy. After confirmation of eradication, endoscopy and a urea breath test were performed yearly. RESULTS: A total of 1,120 patients completed more than 1-yr follow-up and were followed for up to 8.6 yr (a mean of 3.4 yr). Gastric cancer developed in 8 of 944 patients cured of infection and 4 of 176 who had persistent infection (p = 0.04
log-rank test). All the gastric cancer developed in patients with gastric ulcer, but none in patients with duodenal ulcer (p = 0.005
Fisher's exact test). In patients with gastric ulcer, persistent infection was identified as a significant factor for the risk of developing gastric cancer (hazard ratio: 3.35
95% confidence interval: 1.00-11.22
p = 0.04
Cox's proportional-hazards model). CONCLUSION: H. pylori eradication may reduce their risk of developing gastric cancer in patients with gastric ulcer. Large-scale studies in additional populations of this important international public-health issue are warranted. © 2005 by Am. Coll. of Gastroenterology Published by Blackwell Publishing.

DOI： 10.1111/j.1572-0241.2005.41384.x

Neutrophil and lymphocyte responses to oral Streptococcus in Adamantiades-Behçet's disease. 査読

Kurauchi T, Yokota K, Matsuo T, Fujinami Y, Isogai E, Isogai H, Ohtsuki H, Oguma K

FEMS immunology and medical microbiology 43 ( 2 ) 125 - 131 2005年2月

Alteration in the composition of cholesteryl glucosides and other lipids in Helicobacter pylori undergoing morphological change from spiral to coccoid form 査読

Hirofumi Shimomura, Shunji Hayashi, Kenji Yokota, Keiji Oguma, Yoshikazu Hirai

FEMS Microbiology Letters 237 ( 2 ) 407 - 413 2004年8月

記述言語：英語掲載種別：研究論文（学術雑誌）

In this analysis of membrane lipid compositions in Helicobacter pylori, the membrane lipid profiles drastically changed during coccoid formation: cholesteryl-6-O-tetradecanoyl-α-D-glucopyranoside levels increased, cholesteryl-α-D-glucopyranoside and phosphatidyl ethanolamine decreased, and a coordinated increase in cardiolipin and decrease in phosphatidyl glycerol were observed. Cholesteryl-6-O-phosphatidyl-α-D-glucopyranoside was hardly detected in the spiral forms in the logarithmic phase, but subsequently increased throughout the coccoid conversion. These results suggest that environmental stresses induce the expression of certain regulatory systems for lipid metabolism in H. pylori, and that the resulting alterations in lipid composition play an important role in inducing the coccoid conversion. © 2004 Federation of European Microbiological Societies. Published by Elsevier B.V. All rights reserved.

DOI： 10.1016/j.femsle.2004.07.004

Helicobacter pylori Eradication Improves Pre-Existing Reflux Esophagitis in Patients With Duodenal Ulcer Disease 査読

Kuniharu Ishiki, Motowo Mizuno, Susumu Take, Yasuhiro Nagahara, Tomowo Yoshida, Kazuhide Yamamoto, Hiroyuki Okada, Kenji Yokota, Keiji Oguma, Yasushi Shiratori

CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2 ( 6 ) 474 - 479 2004年6月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：ELSEVIER SCIENCE INC

Background & Aims: There has been significant controversy over the relationship between Helicobacter pylori infection and reflux esophagitis. We investigated the effects of eradicating H. pylori on the reflux esophagitis found in patients with peptic ulcers. Methods: Prospective posteradication evaluations were conducted yearly in 162 H. pylori-positive patients who had reflux esophagitis together with peptic ulcer disease (4 women and 158 men, mean age = 49.1 yr). The Los Angeles classification of the patients' esophagitis was: grade A, 90; grade B, 63; and grade C, 9. The follow-up evaluations began 1 to 2 months after completion of the eradication treatment (mean time of follow-up = 22 mo), and consisted of endoscopy and an interview focusing on heartburn. Results: Six patients were withdrawn from the study because of adverse drug reactions or a failure to regularly keep their appointments. After eradication therapy, we observed endoscopically that reflux esophagitis had improved in 87 (55.8%) of the 156 patients. The improvement rate was significantly higher in patients cured of infection (60.8%) than in those with persistent H. pylori infection (38.9%) (P = 0.04). Body mass index (odds ratio = 0.86, 95% confidence interval [CI] = 0.76-0.97), cure of infection (3.68, 95% CI = 1.56-8.69), the absence of a hiatal hernia (3.90, 95% CI = 1.83-8.28), and an ulcer located in the duodenum (2.75, 95% CI = 1.33-5.70) were identified as significant independent factors for the improvement of reflux esophagitis. Conclusions: In patients with reflux esophagitis associated with duodenal ulcer, a significant improvement in pre-existing reflux esophagitis was noted after H. pylori eradication.

DOI： 10.1053/S1542-3565(04)00165-X

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