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.
en-copyright= kn-copyright= en-aut-name=HaqueMahmudul en-aut-sei=Haque en-aut-mei=Mahmudul kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HiraiYoshikazu en-aut-sei=Hirai en-aut-mei=Yoshikazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YokotaKenji en-aut-sei=Yokota en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OgumaKeiji en-aut-sei=Oguma en-aut-mei=Keiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University en-keyword=Helicobacter kn-keyword=Helicobacter en-keyword=steryl glycoside kn-keyword=steryl glycoside en-keyword=cholesteryl glucoside kn-keyword=cholesteryl glucoside END start-ver=1.4 cd-journal=joma no-vol=52 cd-vols= no-issue=1 article-no= start-page=41 end-page=48 dt-received= dt-revised= dt-accepted= dt-pub-year=1998 dt-pub=199802 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Antibody and Cytokine Responses in Helicobacter pylori-Infected Various Mouse Strains en-subtitle= kn-subtitle= en-abstract= kn-abstract=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.
en-copyright= kn-copyright= en-aut-name=DeyAshoka en-aut-sei=Dey en-aut-mei=Ashoka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=YokotaKenji en-aut-sei=Yokota en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KobayashiKeita en-aut-sei=Kobayashi en-aut-mei=Keita kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OgumaKeiji en-aut-sei=Oguma en-aut-mei=Keiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HiraiYoshikazu en-aut-sei=Hirai en-aut-mei=Yoshikazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=AkagiTadaatsu en-aut-sei=Akagi en-aut-mei=Tadaatsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama Univeristy affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University en-keyword=Helicobacter pylori kn-keyword=Helicobacter pylori en-keyword=cytokine kn-keyword=cytokine en-keyword=humoral immunity kn-keyword=humoral immunity en-keyword=cell-mediated immunity kn-keyword=cell-mediated immunity en-keyword=gastritis kn-keyword=gastritis END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=1998 dt-pub=19980630 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Streptococcus sanguis の産生するIgAプロテアーゼとベーチｪット病患者におけるIgA プロテアーゼに対する抗体産生 kn-title=IgA Protease Produced by Streptococcus sanguis and Antibody Production against IgA Protease in Patients with Behcet's Disease en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=横田憲治 kn-aut-sei=横田 kn-aut-mei=憲治 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END start-ver=1.4 cd-journal=joma no-vol=53 cd-vols= no-issue=4 article-no= start-page=193 end-page=200 dt-received= dt-revised= dt-accepted= dt-pub-year=1999 dt-pub=199908 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Molecular typing of enterohemorrhagic Escherichia coli O157:H7 isolated in Okayama Prefecture using pulsed field gel electrophoresis and random amplification of polymorphic DNA. en-subtitle= kn-subtitle= en-abstract= kn-abstract=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.
en-copyright= kn-copyright= en-aut-name=FunamoriYuka en-aut-sei=Funamori en-aut-mei=Yuka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=FujinagaYukako en-aut-sei=Fujinaga en-aut-mei=Yukako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YokotaKenji en-aut-sei=Yokota en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=InoueKaoru en-aut-sei=Inoue en-aut-mei=Kaoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HiraiYoshikazu en-aut-sei=Hirai en-aut-mei=Yoshikazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OgumaKeiji en-aut-sei=Oguma en-aut-mei=Keiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KiraShohei en-aut-sei=Kira en-aut-mei=Shohei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TaketaKazuhisa en-aut-sei=Taketa en-aut-mei=Kazuhisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Jichi Medical School, Tochigi affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University affil-num=8 en-affil= kn-affil=Okayama University en-keyword=molecular epidemiology kn-keyword=molecular epidemiology en-keyword=enterohemorrhagic Escherichia coli O157: H7 kn-keyword=enterohemorrhagic Escherichia coli O157: H7 en-keyword=pulsed field gel electrophoresis kn-keyword=pulsed field gel electrophoresis en-keyword=random amplification of polymorphic DNA kn-keyword=random amplification of polymorphic DNA END start-ver=1.4 cd-journal=joma no-vol=114 cd-vols= no-issue=3 article-no= start-page=325 end-page=327 dt-received= dt-revised= dt-accepted= dt-pub-year=2003 dt-pub=20030131 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=ピロリ菌 (Helicobacter pylori) en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=横田憲治 kn-aut-sei=横田 kn-aut-mei=憲治 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯学総合研究科 病原細菌学 en-keyword=Helicobacter 属 kn-keyword=Helicobacter 属 en-keyword=胃十二指腸疾患 kn-keyword=胃十二指腸疾患 END start-ver=1.4 cd-journal=joma no-vol=14 cd-vols= no-issue=2 article-no= start-page=129 end-page=133 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=20040331 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Antifungal effect of "Mokusaku-Eki" against Trichophyton mentagrophytes and Trichophyton rubrum kn-title=白癬菌に対する木酢液の発育抑制･殺菌作用 en-subtitle= kn-subtitle= en-abstract=The Mokusaku-Eki is a kind of pyroligneous acid and a dark brown colored solution which obtained from the charcoal burner of Quercus spp. woods as a by-product. In Japan, the antifungal effects of this solution are well known in public. However, it is not clear that minimal inhibitory concentration (MIC) of Mokusaku-Eki against Trichophyton spp. In this study, we examined their antifungal activities in view of MIC and germicidal effect. To examine MIC of Mokusaku-Eki against Trichophyton spp, agar, dilution assay were used. Sabouraud agar plates containing 2%, 3%, 4%, or 5% of Mokusaku-Eki were prepared. Then the spores of T. mentagrophytes and T. rubrum inoculated onto each agar plate respectively and incubate the plates at 30℃. The growth of T. mentagrophytes and T. rubrum were completely inhibited on the agar plates contained more than 3% Mokusaku-Eki. Furthermore, we investigated the fungicidal effect of Mokusaku-Eki against these fungus. We exposed the spores of T. mentagrophytes and T. rubrum respectively to 2.5%, 4% or 10% Mokusaku-Eki for 20 min, 1 hr, 6 hr, 24 hr, and 48 hr, and then inoculated them onto Sabouraud agar plates. Exposures of the spores to 5% of the Mokusaku-Eki for 24 hr and 48 hr completely killed them and we could show that Mokusaku-Eki have also germicidation activity against both T. mentagrophytes and T. rubrum. kn-abstract=足白癬は糖尿病患者で合併しやすく,高齢者にも多発する｡近年,白癬菌に対する木酢液の抗菌作用が知られており,この最適有効濃度を明らかにするため本研究を企画した｡白癬菌はTrichophyton mentagrophytesとTrichophyton rubrumの2菌種を用い,木酢液は市販品を用いた｡発育抑制テストは終濃度2,3,4,5%の木酢液を含んだ寒天平板希釈法で行った｡殺菌テストは2.5,5,10%溶液を胞子と接触後,寒天平板培地に接種し,菌の発育の有無を観察した｡発育抑制作用は,両菌種とも3%以上で7日培養後の菌糸の発育は見られなかった｡殺菌作用は, T. mentagrophytesでは10%,5%においては6時間接触で,2.5%においては24時間接触で菌糸の発育が見られず, T. rubrumでは,10%以上においては24時間接触で,5%においては48時間接触で菌糸の発育が見られなかった｡足浴等の看護ケアに木酢液を応用するためには,今後より短時間の接触で効果が得られる方法の検討が必要である｡ en-copyright= kn-copyright= en-aut-name=WatanabeKumi en-aut-sei=Watanabe en-aut-mei=Kumi kn-aut-name=渡邉久美 kn-aut-sei=渡邉 kn-aut-mei=久美 aut-affil-num=1 ORCID= en-aut-name=SumiyoshiKazuko en-aut-sei=Sumiyoshi en-aut-mei=Kazuko kn-aut-name=住吉和子 kn-aut-sei=住吉 kn-aut-mei=和子 aut-affil-num=2 ORCID= en-aut-name=KanekoNoriyo en-aut-sei=Kaneko en-aut-mei=Noriyo kn-aut-name=金子典代 kn-aut-sei=金子 kn-aut-mei=典代 aut-affil-num=3 ORCID= en-aut-name=YokotaKenji en-aut-sei=Yokota en-aut-mei=Kenji kn-aut-name=横田憲治 kn-aut-sei=横田 kn-aut-mei=憲治 aut-affil-num=4 ORCID= en-aut-name=KawataChieko en-aut-sei=Kawata en-aut-mei=Chieko kn-aut-name=川田智惠子 kn-aut-sei=川田 kn-aut-mei=智惠子 aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部保健学科看護学専攻 affil-num=2 en-affil= kn-affil=岡山大学医学部保健学科看護学専攻 affil-num=3 en-affil= kn-affil=岡山大学医学部保健学科看護学専攻 affil-num=4 en-affil= kn-affil=岡山大学大学院医歯学総合研究科病原細菌学 affil-num=5 en-affil= kn-affil=岡山大学医学部保健学科看護学専攻 en-keyword=木酢液 (Mokusaku-Eki) kn-keyword=木酢液 (Mokusaku-Eki) en-keyword=白癬菌 (Trichophyton) kn-keyword=白癬菌 (Trichophyton) en-keyword=発育抑制作用 (Antifungal effect) kn-keyword=発育抑制作用 (Antifungal effect) en-keyword=足部白癬 (Trichophytosis) kn-keyword=足部白癬 (Trichophytosis) END start-ver=1.4 cd-journal=joma no-vol=43 cd-vols= no-issue=2 article-no= start-page=125 end-page=131 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20050201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Neutrophil and lymphocyte responses to oral Streptococcus in Adamantiades-Behcet's disease en-subtitle= kn-subtitle= en-abstract= kn-abstract=Immune reactions against microorganisms play an important pathogenic role in Adamantiades-Beh?et’s disease (ABD). We had previously obtained Streptococcus sanguinis (strain BD113-20) isolated from the oral cavity of patients with ABD. To investigate the pathogenesis of this isolate, we examined neutrophil 5 reactions and level of cytokine production by lymphocytes after stimulation with the strain. The reactions of neutrophils were examined by chemiluminescence assay using whole blood. The amounts of interferon gamma (IFN-g) and interleukin (IL)-4, IL-8, IL-10, and IL-12 produced by peripheral blood mononuclear cells (PBMCs) were measured by ELISA. 10 Strain BD113-20 activated neutrophils from patients with ABD and healthy volunteers, and, in addition it increased IFN-g production by lymphocytes. Lymphocyte from the patients with ABD showed a dominant T helper 1 (Th-1) immune response. Results indicated that both bacterial stimulation and host hypersensitivity might be involved in the symptoms and pathogenesis of ABD. en-copyright= kn-copyright= en-aut-name=KurauchiTomomi en-aut-sei=Kurauchi en-aut-mei=Tomomi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=YokotaKenji en-aut-sei=Yokota en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MatsuoToshihiko en-aut-sei=Matsuo en-aut-mei=Toshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=FujinamiYoshihito en-aut-sei=Fujinami en-aut-mei=Yoshihito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=IsogaiEmiko en-aut-sei=Isogai en-aut-mei=Emiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=IsogaiHiroshi en-aut-sei=Isogai en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OhtsukiHiroshi en-aut-sei=Ohtsuki en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=OgumaKeiji en-aut-sei=Oguma en-aut-mei=Keiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Department of Ophthalmology, Okayama University Graduate School of Medicine and Dentistry affil-num=2 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine and Dentistry affil-num=3 en-affil= kn-affil=Department of Ophthalmology, Okayama University Graduate School of Medicine and Dentistry affil-num=4 en-affil= kn-affil=Department of Ophthalmology, Okayama University Graduate School of Medicine and Dentistry affil-num=5 en-affil= kn-affil=Department of Preventive Dentistry, Health Sciences University of Hokkaido affil-num=6 en-affil= kn-affil=Division of Animal Experimentation, Sapporo Medical University affil-num=7 en-affil= kn-affil=Department of Ophthalmology, Okayama University Graduate School of Medicine and Dentistry affil-num=8 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine and Dentistry en-keyword=Adamantiades-Behcet's disease kn-keyword=Adamantiades-Behcet's disease en-keyword=Streptococcus sanguinis kn-keyword=Streptococcus sanguinis en-keyword=neutrophil kn-keyword=neutrophil en-keyword=chemiluminescence kn-keyword=chemiluminescence en-keyword=IL-8 kn-keyword=IL-8 en-keyword=T helper-1 kn-keyword=T helper-1 en-keyword=IFN-gamma kn-keyword=IFN-gamma en-keyword=IL-12 kn-keyword=IL-12 END start-ver=1.4 cd-journal=joma no-vol=64 cd-vols= no-issue=3 article-no= start-page=163 end-page=170 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=201006 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Passive Oral Immunization by Egg Yolk Immunoglobulin (IgY) to Vibrio cholerae Effectively Prevents Cholera en-subtitle= kn-subtitle= en-abstract= kn-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. en-copyright= kn-copyright= en-aut-name=HiraiKazuyuki en-aut-sei=Hirai en-aut-mei=Kazuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ArimitsuHideyuki en-aut-sei=Arimitsu en-aut-mei=Hideyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=UmedaKoji en-aut-sei=Umeda en-aut-mei=Koji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YokotaKenji en-aut-sei=Yokota en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=ShenLianhua en-aut-sei=Shen en-aut-mei=Lianhua kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=AyadaKiyoshi en-aut-sei=Ayada en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KodamaYoshikatsu en-aut-sei=Kodama en-aut-mei=Yoshikatsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TsujiTakao en-aut-sei=Tsuji en-aut-mei=Takao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=HiraiYoshikazu en-aut-sei=Hirai en-aut-mei=Yoshikazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=OgumaKeiji en-aut-sei=Oguma en-aut-mei=Keiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Microbiology, Fujita Health University, School of Medicine affil-num=3 en-affil= kn-affil=Immunology Research Institute, GHEN Corporation affil-num=4 en-affil= kn-affil=Graduate School of Health Sciences, Okayama University affil-num=5 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Immunology Research Institute, GHEN Corporation affil-num=8 en-affil= kn-affil=Department of Microbiology, Fujita Health University, School of Medicine affil-num=9 en-affil= kn-affil=Division of Infection and Immunuity, Jichi Medical School affil-num=10 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=Vibrio cholerae kn-keyword=Vibrio cholerae en-keyword=O1 kn-keyword=O1 en-keyword=O139 kn-keyword=O139 en-keyword=IgY kn-keyword=IgY END start-ver=1.4 cd-journal=joma no-vol=66 cd-vols= no-issue=3 article-no= start-page=253 end-page=261 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201206 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Clostridium botulinum Type E Toxins Bind to Caco-2 Cells by a Different Mechanism from That of Type A Toxins en-subtitle= kn-subtitle= en-abstract= kn-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. en-copyright= kn-copyright= en-aut-name=ZhangKai en-aut-sei=Zhang en-aut-mei=Kai kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=YamamotoYumiko en-aut-sei=Yamamoto en-aut-mei=Yumiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=SuzukiTomonori en-aut-sei=Suzuki en-aut-mei=Tomonori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YokotaKenji en-aut-sei=Yokota en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MaShaobo en-aut-sei=Ma en-aut-mei=Shaobo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=Nengah Dwi FatmawatiNi en-aut-sei=Nengah Dwi Fatmawati en-aut-mei=Ni kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OgumaKeiji en-aut-sei=Oguma en-aut-mei=Keiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine affil-num=2 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine affil-num=3 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine affil-num=4 en-affil= kn-affil=Graduate School of Health Sciences, Okayama University affil-num=5 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine affil-num=6 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine affil-num=7 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine en-keyword=Clostridum botulinum kn-keyword=Clostridum botulinum en-keyword=neurotoxins kn-keyword=neurotoxins en-keyword=Caco-2 kn-keyword=Caco-2 en-keyword=binding kn-keyword=binding en-keyword=Hc kn-keyword=Hc END start-ver=1.4 cd-journal=joma no-vol=67 cd-vols= no-issue=2 article-no= start-page=93 end-page=98 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201304 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=The Genetic Diversity of Helicobacter pylori Virulence Genes Is Not Associated with Gastric Atrophy Progression en-subtitle= kn-subtitle= en-abstract= kn-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. en-copyright= kn-copyright= en-aut-name=KitaMasahide en-aut-sei=Kita en-aut-mei=Masahide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=YokotaKenji en-aut-sei=Yokota en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OkadaHiroyuki en-aut-sei=Okada en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TakeSusumu en-aut-sei=Take en-aut-mei=Susumu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakenakaRyuta en-aut-sei=Takenaka en-aut-mei=Ryuta kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KawaharaYoshiro en-aut-sei=Kawahara en-aut-mei=Yoshiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OgumaKeiji en-aut-sei=Oguma en-aut-mei=Keiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=MatsushitaOsamu en-aut-sei=Matsushita en-aut-mei=Osamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=YamamotoKazuhide en-aut-sei=Yamamoto en-aut-mei=Kazuhide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Graduate School of Health Sciences, Okayama University affil-num=3 en-affil= kn-affil=Department of Endoscopy, Okayama University Hospital affil-num=4 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=cDepartment of Endoscopy, Okayama University Hospital affil-num=7 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=Helicobacter pylori kn-keyword=Helicobacter pylori en-keyword=virulence genes kn-keyword=virulence genes en-keyword=chronic atrophic gastritis kn-keyword=chronic atrophic gastritis END start-ver=1.4 cd-journal=joma no-vol=14 cd-vols= no-issue= article-no= start-page=1757 end-page=1764 dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=20210512 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Antibacterial Effects of Disulfiram in Helicobacter pylori en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background: Helicobacter pylori infection poses a risk of the occurrence of gastrointestinal diseases, such as gastric cancer. Its incidence rate is significantly reduced by eradication, and thereby, eradication therapy is generally performed. Disulfiram is an oral prescription drug mainly used for the treatment of alcohol dependence. In recent years, reports have been made on its anticancer and antibacterial effects, and thus, it has recently become an interesting subject. This study aimed to examine the antibacterial activity of disulfiram, investigate the presence or absence of its antibacterial activity on H. pylori, and determine whether it could be a new bactericidal drug against drug-resistant H. pylori.