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  • 1
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    Online Resource
    A murine macrophage cell line, immortalized by v‐raf and v‐myc oncogenes, exhibits normal macrophage functions
    Wiley ; 1987
    In:  European Journal of Immunology Vol. 17, No. 10 ( 1987-01), p. 1491-1498
    Details
    In: European Journal of Immunology, Wiley, Vol. 17, No. 10 ( 1987-01), p. 1491-1498
    Abstract: In vitro immortalized cell lines with the morphology and phenotype of mature macrophages (MΦ) have been generated by infecting freshly isolated bone marrow cells from C3H/HeJ mice with a recombinant retrovirus carrying v‐ raf and v‐ myc oncogenes. All of the clones obtained had MΦ‐like phenotypes, and one such clone, GG2EE, has been compared to normal MΦ to ascertain the effects of immortalization on the expression of the biological functions of the lines. GG2EE cells expressed cytotoxic activity against L5178Y, P815 or RL 1 target cells in response to stimulation with interferon‐γ (IFN‐γ) and heat‐killed Listeria monocytogenes ; in contrast, they failed to kill YAC‐1 target cells. GG2EE cells did not constitutively express I‐A or I‐E antigens; nevertheless, I region‐coded antigens could be induced by IFN‐γ treatment. GG2EE cells produced interleukin 1 upon stimulation with a T cell‐derived lymphokine; they were weakly phagocytic, yet became highly phagocytic following IFN‐γ treatment. Since c‐ fos mRNA is augmented in peritoneal exudate MΦ by protein kinase C activators but not by IFN‐γ, we evaluated the effects of calcium ionophore, phorbol myristate acetate, L‐α‐1‐oleoyl‐2‐acetoyl‐sn‐3 glycerol (OAG) and IFN‐γ on the levels of c‐ fos mRNA in GG2EE cells. We found that calcium ionophore, PMA and OAG stimulation enhanced the expression of c‐ fos mRNA, but IFN‐γ treatment did not. The kinetics of c‐ fos induction in GG2EE cells were also comparable to those observed in peritoneal exudate MΦ. Overall, the GG2EE cell line has the same biological properties as normal tissue MΦ. Because it is capable of both constitutive and inducible MΦ‐like functions, this cell line provides a valuable tool for studying the molecular mechanisms controlling induction and/or expression of biological activities in MΦ. It is striking that a cell line immortalized in vitro by two oncogenes, v‐ raf and v‐ myc , behaves, according to the criteria mentioned above, like a normal MΦ population.
    Type of Medium: Online Resource
    ISSN: 0014-2980 , 1521-4141
    URL: Issue
    URL: Article
    DOI: 10.1002/eji.v17:10
    DOI: 10.1002/eji.1830171016
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 1987
    detail.hit.zdb_id: 1491907-2
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  • 2
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    Role of host phosphotyrosine phosphatase SHP-1 in the development of murine leishmaniasis
    Wiley ; 2001
    In:  European Journal of Immunology Vol. 31, No. 11 ( 2001-11), p. 3185-3196
    Details
    In: European Journal of Immunology, Wiley, Vol. 31, No. 11 ( 2001-11), p. 3185-3196
    Type of Medium: Online Resource
    ISSN: 0014-2980 , 1521-4141
    URL: Issue
    URL: Journal
    URL: Article
    DOI: 10.1002/1521-4141(200111)31:11〈〉1.0.CO;2-G
    DOI: 10.1002/(ISSN)1521-4141
    DOI: 10.1002/1521-4141(200111)31:11〈3185::AID-IMMU3185〉3.0.CO;2-J
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2001
    detail.hit.zdb_id: 1491907-2
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  • 3
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    Comparison of the Susceptibilities of C57BL/6 and A/J Mouse Strains to Streptococcus suis Serotype 2 Infection
    American Society for Microbiology ; 2008
    In:  Infection and Immunity Vol. 76, No. 9 ( 2008-09), p. 3901-3910
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 76, No. 9 ( 2008-09), p. 3901-3910
    Abstract: Streptococcus suis is an important swine and human pathogen. Assessment of susceptibility to S. suis using animal models has been limited to monitoring mortality rates. We recently developed a hematogenous model of S. suis infection in adult CD1 outbred mice to study the in vivo development of an early septic shock-like syndrome that leads to death and a late phase that clearly induces central nervous system damage, including meningitis. In the present study, we compared the severities of septic shock-like syndrome caused by S. suis between adult C57BL/6J (B6) and A/J inbred mice. Clinical parameters, proinflammatory mediators, and bacterial clearance were measured to dissect potential immune factors associated with genetic susceptibility to S. suis infection. Results showed that A/J mice were significantly more susceptible than B6 mice to S. suis infection, especially during the acute septic phase of infection (100% of A/J and 16% of B6 mice died before 24 h postinfection). The greater susceptibility of A/J mice was associated with an exaggerated inflammatory response, as indicated by their higher production of tumor necrosis factor alpha, interleukin-12p40/p70 (IL-12p40/p70), gamma interferon, and IL-1β, but not with different bacterial loads in the blood. In addition, IL-10 was shown to be responsible, at least in part, for the higher survival in B6 mice. Our findings demonstrate that A/J mice are very susceptible to S. suis infection and provide evidence that the balance between pro- and anti-inflammatory mediators is crucial for host survival during the septic phase.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00350-08
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2008
    detail.hit.zdb_id: 1483247-1
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  • 4
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    Lipopolysaccharide-Related Stimuli Induce Expression of the Secretory Leukocyte Protease Inhibitor, a Macrophage-Derived Lipopolysaccharide Inhibitor
    American Society for Microbiology ; 1998
    In:  Infection and Immunity Vol. 66, No. 6 ( 1998-06), p. 2447-2452
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 66, No. 6 ( 1998-06), p. 2447-2452
    Abstract: Mouse secretory leukocyte protease inhibitor (SLPI) was recently characterized as a lipopolysaccharide (LPS)-induced product of macrophages that antagonizes their LPS-induced activation of NF-κB and production of NO and tumor necrosis factor (TNF) (F. Y. Jin, C. Nathan, D. Radzioch, and A. Ding, Cell 88:417–426, 1997). To better understand the role of SLPI in innate immune and inflammatory responses, we examined the kinetics of SLPI expression in response to LPS, LPS-induced cytokines, and LPS-mimetic compounds. SLPI mRNA was detectable in macrophages by Northern blot analysis within 30 min of exposure to LPS but levels peaked only at 24 to 36 h and remained elevated at 72 h. Despite the slowly mounting and prolonged response, early expression of SLPI mRNA was cycloheximide resistant. Two LPS-induced proteins—interleukin-10 (IL-10) and IL-6—also induced SLPI, while TNF and IL-1β did not. The slow attainment of maximal induction of SLPI by LPS in vitro was mimicked by infection with Pseudomonas aeruginosa in vivo, where SLPI expression in the lung peaked at 3 days. Two LPS-mimetic molecules—taxol from yew bark and lipoteichoic acid (LTA) from gram-positive bacterial cell walls—also induced SLPI. Transfection of macrophages with SLPI inhibited their LTA-induced NO production. An anti-inflammatory role for macrophage-derived SLPI seems likely based on SLPI’s slowly mounting production in response to constituents of gram-negative and gram-positive bacteria, its induction both as a direct response to LPS and as a response to anti-inflammatory cytokines induced by LPS, and its ability to suppress the production of proinflammatory products by macrophages stimulated with constituents of both gram-positive and gram-negative bacteria.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.66.6.2447-2452.1998
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1998
    detail.hit.zdb_id: 1483247-1
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  • 5
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    Acquired Resistance but Not Innate Resistance to Mycobacterium bovis Bacillus Calmette-Guérin Is Compromised by Interleukin-12 Ablation
    American Society for Microbiology ; 1998
    In:  Infection and Immunity Vol. 66, No. 11 ( 1998-11), p. 5268-5274
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 66, No. 11 ( 1998-11), p. 5268-5274
    Abstract: Interleukin-12 (IL-12) is one of the first cytokines produced by macrophages, key mediators of innate resistance, during the host’s immune response to infections. Therefore, in this study we propose that IL-12 has an important role in the early phase of the immune response to Mycobacterium bovis BCG. IL-12 has been shown to enhance the maturation of protective Th1 cells and gamma interferon (IFN-γ) production during mycobacterial infection. Therefore, it may play a crucial role during the immune phase of infection as well. To examine the role of IL-12 in both the innate and the immune phase of infection, we compared BCG-resistant mice, B10.A ( Bcg r ), to the susceptible congenic strain B10.A ( Bcg s ) following administration of a blocking monoclonal antibody to IL-12 (10F6). Anti-IL-12-treated susceptible animals exhibited a two- to threefold increase in spleen CFU by day 21. In contrast, anti-IL-12 treatment had little or no effect on the response of the genetically resistant animals to infection. The B10.A ( Bcg r ) but not the B10.A ( Bcg s ) mice had an increase in IFN-γ mRNA relative to baseline levels as early as day 1 of infection irrespective of anti-IL-12 treatment. By day 14, B10.A ( Bcg r ) mice showed a decrease in IFN-γ mRNA while the B10.A ( Bcg s ) mice showed a significant increase in IFN-γ mRNA levels. Thus, during BCG infection, the B10.A ( Bcg r ) mice mount an early IFN-γ response against BCG whereas the B10.A ( Bcg s ) mice have a delayed IFN-γ response correlating with their genetic permissiveness expressed as an increased mycobacterial load by day 21. Overall, our data demonstrate that the inherent resistance of B10.A ( Bcg r ) mice to mycobacteria does not depend on optimal levels of IL-12 to maintain effective control of the bacteria, whereas IL-12 is important for the susceptible animals’ response to BCG during the peak of infection.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.66.11.5268-5274.1998
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1998
    detail.hit.zdb_id: 1483247-1
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  • 6
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    Online Resource
    Beneficial effects of secretory leukocyte protease inhibitor after spinal cord injury
    Oxford University Press (OUP) ; 2010
    In:  Brain Vol. 133, No. 1 ( 2010-1), p. 126-138
    Details
    In: Brain, Oxford University Press (OUP), Vol. 133, No. 1 ( 2010-1), p. 126-138
    Type of Medium: Online Resource
    ISSN: 1460-2156 , 0006-8950
    URL: Article
    DOI: 10.1093/brain/awp304
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2010
    detail.hit.zdb_id: 1474117-9
    SSG: 12
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  • 7
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    Differential effector and secretory functions of microglial cell lines derived from BCG-resistant and -susceptible congenic mouse strains
    Elsevier BV ; 1999
    In:  Journal of Neuroimmunology Vol. 101, No. 1 ( 1999-11), p. 27-33
    Details
    In: Journal of Neuroimmunology, Elsevier BV, Vol. 101, No. 1 ( 1999-11), p. 27-33
    Type of Medium: Online Resource
    ISSN: 0165-5728
    URL: Article
    DOI: 10.1016/S0165-5728(99)00127-7
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1999
    detail.hit.zdb_id: 1500497-1
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  • 8
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    Fenretinide Corrects Newly Found Ceramide Deficiency in Cystic Fibrosis
    American Thoracic Society ; 2008
    In:  American Journal of Respiratory Cell and Molecular Biology Vol. 38, No. 1 ( 2008-01), p. 47-56
    Details
    In: American Journal of Respiratory Cell and Molecular Biology, American Thoracic Society, Vol. 38, No. 1 ( 2008-01), p. 47-56
    Type of Medium: Online Resource
    ISSN: 1044-1549 , 1535-4989
    URL: Article
    DOI: 10.1165/rcmb.2007-0036OC
    RVK:
    XA 20260
    Language: English
    Publisher: American Thoracic Society
    Publication Date: 2008
    detail.hit.zdb_id: 1473629-9
    SSG: 12
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  • 9
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    Clearance of Infection with Mycobacterium bovis BCG in Mice Is Enhanced by Treatment with S28463 (R-848), and Its Efficiency Depends on Expression of Wild-Type Nramp1 (Resistance Allele)
    American Society for Microbiology ; 2001
    In:  Antimicrobial Agents and Chemotherapy Vol. 45, No. 11 ( 2001-11), p. 3059-3064
    Details
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 45, No. 11 ( 2001-11), p. 3059-3064
    Abstract: The mouse bcg host resistance gene is known to control the activation of host macrophages for killing of intracellular parasites like Leishmania donovani as well as intracellular bacteria, including Mycobacterium bovis BCG and Salmonella enterica serovar Typhimurium. The Nramp1 gene has been mapped to this locus and affects the efficiency of macrophage activation. It has been shown that imidazoquinoline compounds, including S28463, are able to improve the clearance of a number of intracellular pathogens such as herpes simplex virus 2, human papillomavirus, and Leishmania . The goal of this study was to determine whether S28463 is efficient against infection with another intracellular pathogen, M. bovis BCG, and to determine the molecular basis underlying this effect. To achieve this, B10A. Nramp1 r and B10A. Nramp1 −/− mice were infected with M. bovis BCG and treated with S28463. The bacterial content in the spleen from these mice was assayed by a colony-forming assay. In addition, in vitro experiments were performed using bone marrow-derived macrophage cell lines from these mice. These cells were treated with S28463 and/or gamma interferon (IFN-γ), and nitric oxide (NO) production was measured. Our study was able to show that S28463 acts in synergy with IFN-γ to increase the production of NO in vitro. We were also able to demonstrate that mice that carried the resistant allele of the Nramp1 gene and were infected with M. bovis BCG responded to treatment with S28463, resulting in a decreased bacterial load after 2 weeks of treatment. Mice that do not express the Nramp1 gene responded only to a very large dose of S28463, and the response was not as efficient as that observed in mice carrying a wild-type Nramp1 allele. Our data provide evidence for the potential of S28463 as an immunomodulator that may be helpful in designing efficient strategies to improve host defense against mycobacterial infection.
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    URL: Article
    DOI: 10.1128/AAC.45.11.3059-3064.2001
    RVK:
    XA 24552
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2001
    detail.hit.zdb_id: 1496156-8
    SSG: 12
    SSG: 15,3
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  • 10
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    Hemozoin Increases IFN-γ-Inducible Macrophage Nitric Oxide Generation Through Extracellular Signal-Regulated Kinase- and NF-κB-Dependent Pathways
    The American Association of Immunologists ; 2003
    In:  The Journal of Immunology Vol. 171, No. 8 ( 2003-10-15), p. 4243-4253
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 171, No. 8 ( 2003-10-15), p. 4243-4253
    Abstract: NO overproduction has been suggested to contribute to the immunopathology related to malaria infection. Even though a role for some parasite molecules (e.g., GPI) in NO induction has been proposed, the direct contribution of hemozoin (HZ), another parasite metabolite, remains to be established. Therefore, we were interested to determine whether Plasmodium falciparum (Pf) HZ and synthetic HZ, β-hematin, alone or in combination with IFN-γ, were able to induce macrophage (Mφ) NO synthesis. We observed that neither Pf HZ nor synthetic HZ led to NO generation in B10R murine Mφ; however, they significantly increased IFN-γ-mediated inducible NO synthase (iNOS) mRNA and protein expression, and NO production. Next, by investigating the transductional mechanisms involved in this cellular regulation, we established that HZ induces extracellular signal-regulated kinase (ERK)1/2 mitogen-activated protein kinase phosphorylation as well as NF-κB binding to the iNOS promoter, and enhances the IFN-γ-dependent activation of both second messengers. Of interest, cell pretreatment with specific inhibitors against either NF-κB or the ERK1/2 pathway blocked the HZ + IFN-γ-inducible NF-κB activity and significantly reduced the HZ-dependent increase on IFN-γ-mediated iNOS and NO induction. Even though selective inhibition of the Janus kinase 2/STAT1α pathway suppressed NO synthesis in response to HZ + IFN-γ, HZ alone did not activate this signaling pathway and did not have an up-regulating effect on the IFN-γ-induced Janus kinase 2/STAT1α phosphorylation and STAT1α binding to the iNOS promoter. In conclusion, our results suggest that HZ exerts a potent synergistic effect on the IFN-γ-inducible NO generation in Mφ via ERK- and NF-κB-dependent pathways.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.171.8.4243
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2003
    detail.hit.zdb_id: 1475085-5
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