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  • American Society for Microbiology  (5)
  • 1
    Online Resource
    Online Resource
    A Tetrodotoxin-Producing Vibrio Strain, LM-1, from the Puffer Fish Fugu vermicularis radiatus
    American Society for Microbiology ; 2000
    In:  Applied and Environmental Microbiology Vol. 66, No. 4 ( 2000-04), p. 1698-1701
    Details
    In: Applied and Environmental Microbiology, American Society for Microbiology, Vol. 66, No. 4 ( 2000-04), p. 1698-1701
    Abstract: Identification of tetrodotoxin (TTX) and its derivatives produced from a Vibrio strain in the intestine of the puffer fish Fugu vermicularis radiatus was performed by thin-layer chromatography, electrophoresis, high-performance liquid chromatography, and gas chromatography-mass spectrometry, together with a mouse bioassay for toxicity. It was demonstrated that the isolated bacterium produced TTX, 4-epi-TTX, and anhTTX during cultivation, suggesting that Vibrio strains are responsible for the toxification of the puffer fish.
    Type of Medium: Online Resource
    ISSN: 0099-2240 , 1098-5336
    URL: Article
    DOI: 10.1128/AEM.66.4.1698-1701.2000
    RVK:
    WA 15000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2000
    detail.hit.zdb_id: 223011-2
    detail.hit.zdb_id: 1478346-0
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    CD137 Expressed on Neutrophils Plays Dual Roles in Antibacterial Responses against Gram-Positive and Gram-Negative Bacterial Infections
    American Society for Microbiology ; 2013
    In:  Infection and Immunity Vol. 81, No. 6 ( 2013-06), p. 2168-2177
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 81, No. 6 ( 2013-06), p. 2168-2177
    Abstract: Severe sepsis and septic shock caused mainly by bacterial infections are life-threatening conditions that urge the development of novel therapies. However, host responses to and pathophysiology of sepsis have not been clearly understood, which remains a major obstacle for the development of effective therapeutics. Recently, we have shown that stimulation of a costimulatory molecule, CD137, enhanced survival of mice infected with the Gram-positive (G + ) intracellular bacterium Listeria monocytogenes but decreased survival in a polymicrobial sepsis model. Herein, we report that CD137 deficiency or blocking of CD137 signaling decreased antibacterial responses of mice infected with G + bacteria ( Staphylococcus aureus , Streptococcus pneumoniae , and Enterococcus faecalis ) but increased these responses in mice infected with Gram-negative (G − ) bacteria ( Escherichia coli , Pseudomonas aeruginosa , and Salmonella enterica serovar Typhimurium). Consistent with these findings, stimulation of CD137 by administration of agonistic antibody enhanced responses against G + bacteria, whereas it decreased these responses against G − bacteria. Neutrophils were responsible for CD137-mediated opposite roles in control of G + and G − bacterial infections. Stimulation of CD137 enhanced activities of neutrophils against S. aureus but decreased these activities against E. coli , while CD137 blocking produced opposite results with the stimulation of CD137 in vivo and in vitro . Furthermore, we found that combined signaling of CD137 and Toll-like receptor 2 (TLR2) induced synergistic production of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) by neutrophils, but combined signaling of CD137 and TLR4 did not. Our data strongly suggest that CD137 may play a dual role in sepsis in association with TLRs.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00115-13
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2013
    detail.hit.zdb_id: 1483247-1
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  • 3
    Online Resource
    Online Resource
    Stimulation of the Molecule 4-1BB Enhances Host Defense against Listeria monocytogenes Infection in Mice by Inducing Rapid Infiltration and Activation of Neutrophils and Monocytes
    American Society for Microbiology ; 2009
    In:  Infection and Immunity Vol. 77, No. 5 ( 2009-05), p. 2168-2176
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 77, No. 5 ( 2009-05), p. 2168-2176
    Abstract: The tumor necrosis factor receptor family molecule 4-1BB (CD137) has diverse roles in adaptive and innate immune responses. However, little is known of its role in bacterial infections. Previously, we showed that 4-1BB-deficient mice have enhanced susceptibility to Listeria monocytogenes infection, and mice pretreated with agonistic anti-4-1BB antibody (3E1) were much more resistant to L. monocytogenes infection than mice treated with control antibody. In this study, we report that stimulating 4-1BB by administering 3E1 in the early phase of L. monocytogenes infection is critical for promoting the survival of mice by inducing rapid infiltration of neutrophils and monocytes into L. monocytogenes -infected livers. The levels of tumor necrosis factor alpha, interleukin 6, and monocyte chemoattractant protein 1 in the livers of 3E1-treated mice increased as early as 30 min postinfection and peaked by 1 to 2 h, while those in mice treated with control antibody started to increase only at 16 h postinfection. Monocytes and neutrophils from the 3E1-treated mice had higher levels of activation markers, phagocytic activity, and reactive oxygen species than those from control mice. In vitro stimulation of 4-1BB induced the production of the inflammatory cytokines/chemokines of neutrophils, but not those of monocytes. These results suggest that 4-1BB stimulation of neutrophils in the early phase of L. monocytogenes infection causes rapid production of inflammatory cytokines/chemokines and that the subsequent infiltration of neutrophils and monocytes is crucial for eliminating the infecting L. monocytogenes .
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.01350-08
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2009
    detail.hit.zdb_id: 1483247-1
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  • 4
    Online Resource
    Online Resource
    Blockade of CD137 Signaling Counteracts Polymicrobial Sepsis Induced by Cecal Ligation and Puncture
    American Society for Microbiology ; 2009
    In:  Infection and Immunity Vol. 77, No. 9 ( 2009-09), p. 3932-3938
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 77, No. 9 ( 2009-09), p. 3932-3938
    Abstract: Sepsis, a leading cause of death worldwide, involves proinflammatory responses and inefficient bacterial clearance. Previously, we have shown that CD137 (4-1BB), a member of the tumor necrosis factor receptor superfamily, plays critical roles in eradicating infective Listeria monocytogenes , a gram-positive bacterium, and that stimulation of CD137 protects mice from sepsis-induced death. In this study, we unexpectedly found that CD137 activation aggravated polymicrobial sepsis due to mixed gram-positive and gram-negative bacterial infection induced by cecal ligation and puncture (CLP). CD137-deficient (CD137 −/− ) mice showed significantly lower mortality than CD137-sufficient (CD137 +/+ ) mice in the CLP model. Administration of an agonistic anti-CD137 monoclonal antibody (MAb) to CD137 +/+ mice decreased their survival in this infection model, while administration of a blocking anti-CD137 ligand MAb (TKS-1) to such mice increased their survival. CD137 −/− mice and TKS-1-treated CD137 +/+ mice had lower levels of chemokines/proinflammatory cytokines (monocyte chemoattractant protein 1, interleukin-6 [IL-6], tumor necrosis factor alpha, IL-12) and an anti-inflammatory cytokine (IL-10), exhibited improved bacterial clearance in the peritoneum, liver, and blood, and had greater numbers of infiltrated peritoneal neutrophils and macrophages in the CLP model than control mice. Our data suggest that CD137 activation aggravates polymicrobial sepsis induced by CLP.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00407-09
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2009
    detail.hit.zdb_id: 1483247-1
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  • 5
    Online Resource
    Online Resource
    Activation of NLRP3 and AIM2 Inflammasomes by Porphyromonas gingivalis Infection
    American Society for Microbiology ; 2014
    In:  Infection and Immunity Vol. 82, No. 1 ( 2014-01), p. 112-123
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 82, No. 1 ( 2014-01), p. 112-123
    Abstract: Porphyromonas gingivalis , a major periodontopathogen, is involved in the pathogenesis of periodontitis. Interleukin-1β (IL-1β), a proinflammatory cytokine, regulates innate immune responses and is critical for the host defense against bacterial infection. However, excessive IL-1β is linked to periodontal destruction. IL-1β synthesis, maturation, and secretion are tightly regulated by Toll-like receptor (TLR) signaling and inflammasome activation. We found much higher levels of inflammasome components in the gingival tissues from patients with chronic periodontitis than in those from healthy controls. To investigate the molecular mechanisms by which P. gingivalis infection causes IL-1β secretion, we examined the characteristics of P. gingivalis -induced signaling in differentiated THP-1 cells. We found that P. gingivalis induces IL-1β secretion and inflammatory cell death via caspase-1 activation. We also found that P. gingivalis -induced IL-1β secretion and pyroptic cell death required both NLRP3 and AIM2 inflammasome activation. The activation of the NLRP3 inflammasome was mediated by ATP release, the P2X 7 receptor, and lysosomal damage. In addition, we found that the priming signal via TLR2 and TLR4 activation precedes P. gingivalis -induced IL-1β release. Our study provides novel insight into the innate immune response against P. gingivalis infection which could potentially be used for the prevention and therapy of periodontitis.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00862-13
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2014
    detail.hit.zdb_id: 1483247-1
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