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  • S. Karger AG  (4)
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  • S. Karger AG  (4)
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  • 1
    In: Neuroimmunomodulation, S. Karger AG, Vol. 22, No. 3 ( 2015), p. 203-212
    Abstract: 〈 b 〉 〈 i 〉 Objectives: 〈 /i 〉 〈 /b 〉 Vasoactive intestinal peptide (VIP) is an immunomodulatory neuropeptide with therapeutic properties in multiple murine models of inflammatory disease including the trinitrobenzene-sulfonic acid (TNBS)-colitis model of Crohn's disease. Understanding the spectrum of biological actions of endogenously produced VIP may help us dissect the complex and multifactorial pathogenesis of such inflammatory diseases. Our goal was to determine the contribution of endogenously produced VIP to TNBS-colitis by using VIP knockout (KO) mice. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 TNBS was intracolonically administered to wild-type (WT) and VIP KO mice, and weight loss and colitis were assessed over time. Colon histopathological changes and myeloperoxidase activities were analyzed and the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in colon and serum quantified. The proliferative response in vitro of splenocytes from TNBS WT and VIP KO administered mice to anti-CD3 and anti-CD28 was determined. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 VIP KO mice did not exhibit the predicted exacerbated response to TNBS. Instead, they developed a milder clinical profile than WT mice, with lower TNF-α and IL-6 levels. Such potential defects seem selective, because other parameters such as the histopathological scores and the cytokine levels in the colon did not differ between the two strains of mice. Moreover, splenocytes from TNBS-treated VIP KO mice exhibited an enhanced proliferative response to anti-CD3/CD28 stimulation in vitro. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 Chronic loss of VIP in mice leads to a disruption of certain but not all immunological compartments, corroborating recent findings that VIP KO mice exhibit reduced mortality in the lipopolysaccharide-induced endotoxemia model and attenuated clinical development of experimental autoimmune encephalomyelitis while developing robust T-cell responses.
    Type of Medium: Online Resource
    ISSN: 1021-7401 , 1423-0216
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 1483035-8
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  • 2
    Online Resource
    Online Resource
    S. Karger AG ; 2008
    In:  Neuroendocrinology Vol. 88, No. 4 ( 2008), p. 246-255
    In: Neuroendocrinology, S. Karger AG, Vol. 88, No. 4 ( 2008), p. 246-255
    Abstract: 〈 i 〉 Background/Aims: 〈 /i 〉 Circadian control of behavior and physiology is a central characteristic of all living organisms. The master clock in mammals resides in the hypothalamus, where the suprachiasmatic nucleus (SCN) synchronizes daily rhythms. A variety of recent evidence indicates that the neuropeptide vasoactive intestinal peptide (VIP) is critical for normal functioning of the SCN. The aim of our study was to examine the possible role of VIP in driving circadian rhythms in the hypothalamic-pituitary-adrenal axis. 〈 i 〉 Methods: 〈 /i 〉 Circulating ACTH and corticosterone concentrations were determined by round-the-clock sampling under diurnal and circadian conditions. The responsive aspects of the hypothalamic-pituitary-adrenal axis were tested by application of acute stress by footshock and light. 〈 i 〉 Results: 〈 /i 〉 We demonstrate that the circadian rhythms in ACTH and corticosterone are lost in VIP-deficient mice. The ability of light to induce a corticosterone response was also compromised in the mutant mice, as was photic induction of 〈 i 〉 Per1 〈 /i 〉 in the adrenal glands. In contrast, the acute stress response was apparently unaltered by the loss of VIP. 〈 i 〉 Conclusion: 〈 /i 〉 Thus, our data demonstrate that VIP is essential for the circadian regulation of an otherwise intact hypothalamic-pituitary-adrenal axis.
    Type of Medium: Online Resource
    ISSN: 0028-3835 , 1423-0194
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2008
    detail.hit.zdb_id: 1483028-0
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  • 3
    Online Resource
    Online Resource
    S. Karger AG ; 1995
    In:  Developmental Neuroscience Vol. 17, No. 1 ( 1995), p. 1-7
    In: Developmental Neuroscience, S. Karger AG, Vol. 17, No. 1 ( 1995), p. 1-7
    Type of Medium: Online Resource
    ISSN: 1421-9859 , 0378-5866
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1995
    detail.hit.zdb_id: 1482201-5
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  • 4
    Online Resource
    Online Resource
    S. Karger AG ; 2002
    In:  Developmental Neuroscience Vol. 24, No. 1 ( 2002), p. 14-23
    In: Developmental Neuroscience, S. Karger AG, Vol. 24, No. 1 ( 2002), p. 14-23
    Abstract: Pituitary adenylyl cyclase activating peptide (PACAP) is widely expressed in the embryonic brain at the onset of neurogenesis, and is strongly upregulated in several models of nerve injury. Moreover, high-affinity PACAP receptors are expressed in proliferative zones in the embryonic and postnatal nervous system suggesting that PACAP regulates the development of both neuronal and glial precursors. Tissue culture studies indicate that PACAP exerts a variety of growth factor-like actions that depend on the origin of the cell population and developmental stage. These effects include regulation of proliferation, survival, maturation, neurite outgrowth, and expression of trophic factors, cytokines and trk receptors. The presence of other growth factors can also markedly affect these actions of PACAP, for example, reversing PACAP’s effect from proliferative to antiproliferative. In vivo models now provide additional evidence that PACAP acts in neural development and regeneration.
    Type of Medium: Online Resource
    ISSN: 0378-5866 , 1421-9859
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2002
    detail.hit.zdb_id: 1482201-5
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