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  • 1
    Electronic Resource
    Electronic Resource
    Neuropeptides in the livers of mice during bacterial infections (1998)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 20 (1998), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Neuropeptides such as substance P (SP) and vasoactive intestinal peptide (VIP) are known to act as immunomodulators. We investigated the induction of SP and VIP in the livers of mice infected with Listeria monocytogenes or injected with Tsukamurella paurometabolum. VIP was detected in the livers of mice after L. monocytogenes infection by an immunohistochemical technique and preproVIP mRNA, which was detected by reverse transcription-polymerase chain reaction (PCR), was induced post infection. However, no SP was detected. In contrast, SP, but not VIP was detected within granulomas in the livers of T. paurometabolum-injected mice, suggesting VIP and SP might be selectively induced in the liver by different bacterial infections.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1998.tb01123.x
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  • 2
    Electronic Resource
    Electronic Resource
    Roles of endogenous cytokines in liver apoptosis of mice in lethal Listeria monocytogenes infection (2000)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 28 (2000), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Various bacterial pathogens have been identified as mediators of apoptosis. Apoptosis reportedly shows both detrimental and beneficial effects on biological functions. We studied the role of liver apoptosis in lethal Listeria monocytogenes infection and the regulation of apoptosis by endogenous cytokines during infection. Apoptosis was observed in the spleen but not in the liver of infected mice, whereas the induction of liver necrosis was evident by rising levels of serum aminotransferases in these animals. Apoptosis was detected in the liver of L. monocytogenes-infected mice which had been treated with monoclonal antibody (mAb) against tumor necrosis factor-α (TNF-α) or interleukin-6 (IL-6), or in TNF-α−/− mice, but not in γ- interferon (IFN-γ)−/− mice or mice which had been treated with mAb against IL-4 or IL-10. Augmentation of liver apoptosis in mice treated with mAb against TNF-α or IL-6 or in TNF-α−/− mice correlated with the increase in bacterial numbers in the organ, while no augmentation of apoptosis was observed in the liver of IFN-γ−/− mice irrespective of the marked increase in bacterial numbers in the organs, indicating that augmentation of liver apoptosis may not be merely due to the increase in bacterial growth in the organs. These results suggest that TNF-α and IL-6 may play an important role in protecting the liver from apoptosis in lethal L. monocytogenes infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.2000.tb01495.x
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  • 3
    Electronic Resource
    Electronic Resource
    Erratum to: “Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice” (1999)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 25 (1999), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1999.tb01366.x
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  • 4
    Electronic Resource
    Electronic Resource
    Studies on the functional site on staphylococcal enterotoxin A responsible for production of murine gamma interferon (1999)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 25 (1999), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: To identify the functional region(s) associated with induction of gamma interferon on the staphylococcal enterotoxin A molecule, native staphylococcal enterotoxin A molecules and 12 various synthetic peptides corresponding to different regions of entire staphylococcal enterotoxin A were compared to induce gamma interferon production in murine spleen cells. The native staphylococcal enterotoxin A molecule induced gamma interferon production, whereas all of the 12 synthetic peptides did not. Pre-treatment of the murine spleen cells with synthetic peptide A-9 (corresponding to amino acid residues 161–180) significantly inhibited the staphylococcal enterotoxin A-induced gamma interferon production, whereas those with other synthetic peptides did not. When native staphylococcal enterotoxin A was pre-treated with either anti-staphylococcal enterotoxin A serum or anti-peptide sera, anti-staphylococcal enterotoxin A serum and antisera to peptides A-1 (1–20), A-7 (121–140), A-8 (141–160), A-9 (161–180) and A-10 (181–200) inhibited the staphylococcal enterotoxin A-induced gamma interferon production. From these findings, the amino acid residues 161–180 on the staphylococcal enterotoxin A molecule may be an essential region for murine gamma interferon production. Furthermore, the neutralizing epitopes may be also located on regions of amino acid residues 1–20, 121–140, 141–160 and 181–200 on the staphylococcal enterotoxin A molecule.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1999.tb01348.x
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  • 5
    Electronic Resource
    Electronic Resource
    Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice (1999)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS microbiology letters 175 (1999), S. 0 
    Details
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: It has been demonstrated that endogenous cytokines including γ interferon (IFN-γ), tumour necrosis factor-α (TNF-α), and interleukin-6 (IL-6) play protective roles but that IL-4 and IL-10 play detrimental roles in nonlethal Listeria monocytogenes infection in mice. In this paper, we studied the roles of endogenous cytokines in a lethal infection with L. monocytogenes in mice. TNF-α and IL-6 titres in the bloodstreams, spleens and livers paralleled bacterial numbers in the organs, and both these cytokines and the bacterial numbers peaked just before the mice died. The high titres of TNF-α notably detected in the circulation in lethal infection were different from those in nonlethal infection. The maximum production of IFN-γ was observed before the peaks of TNF-α and IL-6, and IFN-γ almost disappeared from the bloodstreams and organs just before the mice died. No notable difference of IFN-γ titres between lethal infection and nonlethal infection in the specimens obtained from mice was observed. IL-10 was also detected in the bloodstreams earlier than the peaks of TNF-α and IL-6 during lethal infection, while IL-4 was never detected in the sera. The administration of monoclonal antibodies (mAbs) against TNF-α, IFN-γ, IL-6, IL-4 or IL-10 failed to rescue mice from lethal L. monocytogenes infection, whereas anti-TNF-α mAb and anti-IFN-γ mAb prevented mice from lethality by high-dose endotoxin shock. These results suggest that lethality in L. monocytogenes infection might not be determined solely by these cytokines.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-6968.1999.tb13612.x
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  • 6
    Electronic Resource
    Electronic Resource
    The protective role of endogenous cytokines in host resistance against an intragastric infection with Listeria monocytogenes in mice (1996)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 16 (1996), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Abstract It has been demonstrated that endogenous cytokines including gamma-interferon (IFN-γ), tumour necrosis factor-α (TNF-α), and interleukin-6 (IL-6) play a protective role but that IL-4 plays a detrimental role in systemic Listeria monocytogenes infection in mice. The diverse roles of IL-10 have been reported in antilisterial resistance. In this paper, we studied the role of endogenous cytokines in host resistance against an intragastric infection with L. monocytogenes in mice. The expression of cytokine mRNAs including IFN-γ, TNF-α, IL-4, IL-6, or IL-10, which were amplified by reverse transcription-PCR, was observed in intestinal intraepithelial lymphocytes irrespective of L. monocytogenes infection. Increased numbers of L. monocytogenes were detected in the ileal contents of infected mice which received monoclonal antibodies (mAbs) against IFN-γ, TNF-α, IL-4, IL-6, or IL-10. By contrast, mAbs against IL-4 or IL-6 showed little effect on the growth of L. monocytogenes in the mesenteric lymph nodes (MLNs), spleen, and liver, but anti-IFN-γ mAb and anti-TNF-α mAb suppressed the defense in these organs. Anti-IL-10 mAb enhanced bacterial elimination from the MLNs but not from the spleen or liver. These results suggest that the role of endogenous cytokines may differ between systemic and intestinal defenses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1996.tb00148.x
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  • 7
    Electronic Resource
    Electronic Resource
    A monoclonal antibody against T-cell receptor αβ induces endogenous cytokines and prevents mice from a lethal infection with Listeria monocytogenes (1995)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 11 (1995), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Abstract In vivo induction of cytokines by a monoclonal antibody (mAb) against T-cell receptor (TCR) αβ and the protective effect induced by the mAb on a lethal infection with Listeria monocytogenes were studied. Injection of anti-TCR αβ mAb induced rapid production of endogenous tumour necrosis factor in the spleens, and gamma interferon and interleukin-6 in the bloodstreams and spleens of mice. Administration of anti-CD4 mAb, anti-CD8 mAb, or anti-Thy1.2 mAb resulted in suppression of anti-TCR αβ mAb-induced endogenous cytokine production. Mice were protected against lethal L. monocytogenes infection when treated with anti-TCR αβ mAb. The protective effect was not demonstrated in CD4 + cell- or CD8 + cell-depleted mice. These results suggest that anti-TCR αβ mAb shows a protective effect on a lethal infection with L. monocytogenes in mice and that the mAb-induced endogenous cytokines might be involved in the effect of anti-TCR αβ mAb.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1995.tb00162.x
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  • 8
    Electronic Resource
    Electronic Resource
    Dysregulation of interleukin-10 and interleukin-12 are involved in the reduced host resistance to Listeria monocytogenes infection in alymphoplastic aly mutant mice (2002)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 32 (2002), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The aly is a unique spontaneous autosomal recessive mutation in mice that causes a systemic defect of lymph nodes and Peyer's patches and disorganized splenic and thymic structures with immunodeficiency. Our previous study demonstrated that resistance to Listeria monocytogenes infection and interferon-γ (IFN-γ) production are attenuated in the mutant mice. In this study, we investigated the mechanism of decrease in antilisterial resistance and IFN-γ production in aly mice. Interleukin (IL)-12 production in response to heat-killed L. monocytogenes (HK-LM) was decreased but IL-10 production was increased in aly/aly macrophage cultures, compared with those in aly/+ macrophages. Nonadherent cells and macrophages obtained from the spleens of naive aly/+ mice and aly/aly mice were reconstituted and stimulated with HK-LM. IFN-γ production was markedly decreased when macrophages derived from aly/aly mice were used. IFN-γ production in aly/aly spleen cell cultures was recovered in the presence of anti-IL-10 monoclonal antibody (mAb) or recombinant IL-12. When aly/+ mice and aly/aly mice were injected with mAb against IL-10 or IL-12 p40, antilisterial resistance was inhibited by injection of anti-IL-12 p40 mAb, while anti-IL-10 mAb treatment augmented the resistance. Administration of anti-IFN-γ mAb attenuated antilisterial resistance in aly/+ mice but not in aly/aly mice. The present results suggest that downregulation of IL-12 and upregulation of IL-10 in macrophages might be involved in the decrease in antilisterial resistance and IFN-γ production in aly/aly mice in addition to the structural defect in lymphoid organs. Moreover, the results predict that an IL-12-dependent and IFN-γ-independent mechanism may be also involved in the decrease in antilisterial resistance in aly/aly mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.2002.tb00542.x
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