JaLCDOI 10.18926/AMO/49667
FullText URL 67_2_93.pdf
Author Kita, Masahide| Yokota, Kenji| Okada, Hiroyuki| Take, Susumu| Takenaka, Ryuta| Kawahara, Yoshiro| Oguma, Keiji| Matsushita, Osamu| Yamamoto, Kazuhide|
Abstract Atrophy of the gastric mucosa is a precursor of intestinal-type gastric cancer, and Helicobacter pylori infection causes atrophic gastritis. The aim of this study was to determine whether the genetic diversity of H. pylori virulence genes is associated with the development and progression of gastric atrophy in humans. We isolated and cultured H. pylori strains from patients with gastric ulcer and duodenal ulcer accompanied by atrophic gastritis in background mucosa. H. pylori strains were stored at -80℃ prior to the experiments being carried out. We analyzed iceA, babA, vacA, cagA, and cagE genes by PCR. The cagA gene was analyzed through sequencing of the C-terminal region containing the EPIYA motif, which is related to tyrosine phosphorylation. Severe atrophy was observed in patients with gastric ulcer. The major phenotype of the vacA gene was s1c/m1 (93オ). The cagA gene was detected in all strains. The cagE gene was not detected in 2 and 5 strains from the mild cases and severe cases, respectively. The major cagA EPIYA motif, which is amino acids repeat in the C terminus, was the A-B-D type (44 of 58 strains). The virulence genes were not statistically associated with the severity of atrophy in the background gastric mucosa in humans. Not only identification of bacterial virulence factors but also studies of the host response will be necessary to investigate the progression of gastric atrophy and subsequent cancer development in humans.
Keywords Helicobacter pylori virulence genes chronic atrophic gastritis
Amo Type Original Article
Published Date 2013-04
Publication Title Acta Medica Okayama
Volume volume67
Issue issue2
Publisher Okayama University Medical School
Start Page 93
End Page 98
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2013 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 23603925
Web of Sience KeyUT 000317801700003
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/52508
JaLCDOI 10.18926/AMO/48565
FullText URL 66_3_253.pdf
Author Zhang, Kai| Yamamoto, Yumiko| Suzuki, Tomonori| Yokota, Kenji| Ma, Shaobo| Nengah Dwi Fatmawati, Ni| Oguma, Keiji|
Abstract Cultured Clostridium botulinum strains produce progenitor toxins designated as 12S, 16S, and 19S toxins. The 12S toxin consists of a neurotoxin (NTX, 7S) and a non-toxic non-hemagglutinin (NTNH). The 16S and 19S toxins are formed by conjugation of the 12S toxin with hemagglutinin (HA), and the 19S toxin is a dimer of the 16S toxin. Type A cultures produce all 3 of these progenitor toxins, while type E produces only the 12S toxin. The 7S toxin is cleaved into heavy (H) and light (L) chains by a protease(s) in some strains, and the H chain has 2 domains, the N-terminus (Hn) and C-terminus (Hc). It has been reported that type A toxins bind to the intestinal cells or cultured cells via either HA or Hc. In this study, we investigated the binding of type A and E toxins to Caco-2 cells using Western blot analysis. Both the type E 7S and 12S toxins bound to the cells, with the 7S toxin binding more strongly, whereas, in the type A strain, only the 16S/19S toxins showed obvious binding. Pre-incubation of the type E 7S toxin with IgG against recombinant type E Hc significantly inhibited the 7S toxin binding, indicating that Hc might be a main binding domain of the type E toxin.
Keywords Clostridum botulinum neurotoxins Caco-2 binding Hc
Amo Type Original Article
Published Date 2012-06
Publication Title Acta Medica Okayama
Volume volume66
Issue issue3
Publisher Okayama University Medical School
Start Page 253
End Page 261
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22729106
Web of Sience KeyUT 000305669700009
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/48451
JaLCDOI 10.18926/AMO/40008
FullText URL fulltext.pdf
Author Hirai, Kazuyuki| Arimitsu, Hideyuki| Umeda, Koji| Yokota, Kenji| Shen, Lianhua| Ayada, Kiyoshi| Kodama, Yoshikatsu| Tsuji, Takao| Hirai, Yoshikazu| Oguma, Keiji|
Abstract In an attempt to prepare egg yolk immunoglobulin (IgY) to treat and prevent cholera, hens were immunized by a mixture of heat- or formalin-killed Vibrio cholerae O1 and O139 organisms, or by the recombinant cholera toxin B subunit (CTB). The IgYs were partially purified from egg yolk and orally administered to suckling mice before or after challenge with live O1 or O139 cells. The anti-O1 and O139 IgYs and the mixture of either IgY with anti-CTB IgY significantly protected the occurrence of cholera caused by both O1 and O139 infection. Since large amounts of IgY can be prepared very easily and at low cost, this seems to be a useful procedure for preventing and treating cholera.
Keywords Vibrio cholerae O1 O139 IgY
Amo Type Original Article
Published Date 2010-06
Publication Title Acta Medica Okayama
Volume volume64
Issue issue3
Publisher Okayama University Medical School
Start Page 163
End Page 170
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 20596127
Web of Sience KeyUT 000279094300002
Author Kurauchi, Tomomi| Yokota, Kenji| Matsuo, Toshihiko| Fujinami, Yoshihito| Isogai, Emiko| Isogai, Hiroshi| Ohtsuki, Hiroshi| Oguma, Keiji|
Published Date 2005-02-01
Publication Title FEMS Immunology and Medical Microbiology
Volume volume43
Issue issue2
Content Type Journal Article
JaLCDOI 10.18926/AMO/31612
FullText URL fulltext.pdf
Author Funamori, Yuka| Fujinaga, Yukako| Yokota, Kenji| Inoue, Kaoru| Hirai, Yoshikazu| Oguma, Keiji| Kira, Shohei| Taketa, Kazuhisa|
Abstract <p>Three outbreaks and many isolated cases of enterohemorrhagic Escherichia coli O157:H7 occurred in 1996 and 1997 in Okayama Prefecture, Japan. In an attempt to investigate the route of these infections, the strains isolated from the 3 outbreaks (total 33 strains) and 15 isolated cases (total 15 strains) were investigated using random amplification of polymorphic DNA (RAPD) and pulsed-field gel electrophoresis (PFGE). In addition, 10 strains from an outbreak in Tojo Cho, Hiroshima Prefecture (June 1996), 2 strains from the particular types of meat in Kochi Prefecture, and 42 strains isolated from bovine feces in a farm in Okayama Prefecture were also investigated in the same manner. PFGE was much more useful than RAPD for molecular typing of the clinical isolates, in that it allowed us to classify them into 10 PFGE groups. We noted that the strains differed according to the time and place of the outbreaks (or isolated cases). This indicates that O157:H7 infections in Okayama Prefecture were caused by different strains (although some cases were aggravated by the same strains as were found in other areas). The isolates from bovine feces were classified into 5 groups by PFGE profiles, but none of them were identical to those of the clinical isolates.</p>
Keywords molecular epidemiology enterohemorrhagic Escherichia coli O157: H7 pulsed field gel electrophoresis random amplification of polymorphic DNA
Amo Type Article
Published Date 1999-08
Publication Title Acta Medica Okayama
Volume volume53
Issue issue4
Publisher Okayama University Medical School
Start Page 193
End Page 200
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 10488407
Web of Sience KeyUT 000082334300006
JaLCDOI 10.18926/AMO/31337
FullText URL fulltext.pdf
Author Dey, Ashoka| Yokota, Kenji| Kobayashi, Keita| Oguma, Keiji| Hirai, Yoshikazu| Akagi, Tadaatsu|
Abstract <p>Helicobacter pylori (H. pylori) infection in the stomach is etiologically closely associated with chronic active gastritis, peptic ulcer, gastric cancer and gastric mucosa-associated lymphoid tissue lymphoma. In this study, we examined the antibody responses and cytokine profiles of three strains of mice (BALB/c, C3H/He, and C57BL/6) infected with H. pylori. Following this, correlations between host-immune reactions and intensity of inflammation were analyzed. H. pylori (ATCC43504) was intragastrically administered once a week to the mice from 4 weeks of age, and they were sacrificed at the ages of 4 and 7 months. In these mice, we examined the histology of the stomach, antibody titers against H. pylori, and serum levels of cytokines (IL-4, IL-10, TNF-alpha, IL-2 and Interferon-gamma). In BALB/c mice, inflammation of the stomach was minimal. Inflammation was observed in 63.6% of C57BL/6 mice and 33.3% of C3h/He mice. In C57BL/6 and C3H/He mice, all the cytokines tended to increase. In contrast, BALB/c mice were inactive in cytokine production except for IL-2. Two C3H/He mice developed severe inflammation with lymph follicles; one showed a response largely typical of Th-1, and the other showed a response largely typical of Th-2. Although a definite correlation was not shown between Th-1/Th-2 response evaluated by cytokine production and intensity of inflammation, it appears that in H. pylori-induced inflammation both cell-mediated (Th-1) and humoral (Th-2) immunity play a role in pathogenesis.</p>
Keywords Helicobacter pylori cytokine humoral immunity cell-mediated immunity gastritis
Amo Type Article
Published Date 1998-02
Publication Title Acta Medica Okayama
Volume volume52
Issue issue1
Publisher Okayama University Medical School
Start Page 41
End Page 48
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 9548993
Web of Sience KeyUT 000072264100006
JaLCDOI 10.18926/AMO/30380
FullText URL fulltext.pdf
Author Haque, Mahmudul| Hirai, Yoshikazu| Yokota, Kenji| Oguma, Keiji|
Abstract <p>Many of Helicobacter species have been found to have novel cholesteryl glucosides (CGs). To study the biosynthetic mechanism of CGs, the lipid profiles of H. pylori and H. mustelae grown in serum-supplemented and cholesterol-restricted serum-free media were investigated. In contrast to the serum-supplemented state, helicobacters had less CGs in the serum-free state; a trace amount of CGs and no CG was detected in H. pylori and H. mustelae, respectively. The proportion of total and individual phospholipid also showed significant alteration. Unknown lipids which did not contain phosphate and sugar were detected in the serum-free state, but not in the serum-supplemented state. The CGs were found to be distributed mainly in the membrane fractions, and one of the unknown lipids was found exclusively in the cytosol fraction. Based on these data, it is apparent that the CGs of helicobacters are synthesized by de novo uptake of cholesterol from the media. The unknown lipids detected in the serum-free state may be storage lipids, appearing in response to depletion of nutrients, especially cholesterol, or other factors in the media.</p>
Keywords Helicobacter steryl glycoside cholesteryl glucoside
Amo Type Article
Published Date 1995-08
Publication Title Acta Medica Okayama
Volume volume49
Issue issue4
Publisher Okayama University Medical School
Start Page 205
End Page 211
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 7502681
Web of Sience KeyUT A1995RR97800005
Author Watanabe, Kumi| Sumiyoshi, Kazuko| Kaneko, Noriyo| Yokota, Kenji| Kawata, Chieko|
Published Date 2004-03-31
Publication Title 岡山大学医学部保健学科紀要
Volume volume14
Issue issue2
Content Type Departmental Bulletin Paper
Author 横田 憲治|
Published Date 2003-01-31
Publication Title 岡山医学会雑誌
Volume volume114
Issue issue3
Content Type Journal Article
Author 横田 憲治|
Published Date 1998-06-30
Publication Title
Content Type Thesis or Dissertation