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  • 1
    Electronic Resource
    Electronic Resource
    Substance P induction of murine keratinocyte PAM 212 interleukin 1 production is mediated by the neurokinin 2 receptor (NK-2R) (2000)
    Copenhagen : Munksgaard International Publishers
    Experimental dermatology 9 (2000), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The neurological system plays an important role in modulating some inflammatory skin diseases. Neuro-cutaneous interactions may be mediated by the release of neuropeptides such as substance P (SP) which activate immunocompetent cells in the skin by binding to high affinity neurokinin receptors (NKR). Since epidermal keratinocytes produce a variety of cytokines and are intimately associated with cutaneous sensory fibers, we tested the ability of these cells to participate in the cutaneous neuroimmune system by the secretion of potent cytokines such as interleukin 1 (IL-1) in response to released SP. RT-PCR studies demonstrated that cultured PAM 212 murine keratinocytes expressed mRNA for NK-2R but not NK-1R. Correspondingly, the addition of SP to these cells resulted in a rapid increase in intracellular Ca2+ levels that could be specifically blocked by an NK-2R antagonist. NK-2R was also shown in normal mouse epidermis by immunohistochemistry. SP augmented the expression of PAM 212 keratinocyte IL-1α mRNA in a dose and time dependent manner and this induction was inhibited by an NK-2R antagonist. Secretion of bioactive IL-1α by the PAM 212 keratinocytes was likewise stimulated by SP in a dose dependent manner. These data support the hypothesis that SP released from cutaneous sensory nerves contributes to neuroimmune inflammatory responses in the skin by modulating the expression and release of cytokines from epidermal keratinocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0625.2000.009001042.x
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  • 2
    Electronic Resource
    Electronic Resource
    In Vivo human melanoma cytokine production: Inverse correlation of GM-CSF production with tumor depth (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Experimental dermatology 7 (1998), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Melanomas produce multiple cytokines which may influence their growth in vivo. Experimental evidence suggests that granulocyte macrophage-colony stimulating factor (GM-CSF) can induce a potent anti-melanoma response, whereas interleukin-8 (IL-8) may act as a growth factor in human melanoma. Little is currently known regarding the production of these cytokines by human melanoma in vivo. In this study we tested the hypothesis that endogenous production of GM-CSF and IL-8 can be correlated with the depth of human malignant melanoma surgical specimens. We examined 45 melanocytic human tissue samples consisting of 27 primary cutaneous melanomas, 9 metastatic melanomas, and 9 dysplastic nevi for in vivo GM-CSF and IL-8 production using immunohistochemistry. The majority of thin melanomas (≤0.76 mm) stained highly positive for GM-CSF with little or no staining for IL-8 whereas the medium (≤0.76 –≤4.0 mm) and thick (〉4.0 mm) melanoma specimens showed little or no staining for GM-CSF and significant amounts of IL-8 staining. Metastatic melanoma as well as dysplastic nevi specimens had little or no GM-CSF and IL-8 staining. These results support the hypothesis that endogenous melanoma cytokines such as GM-CSF and IL-8 with opposing effects on tumor progression play an important role in melanoma growth and regulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0625.1998.tb00333.x
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  • 3
    Electronic Resource
    Electronic Resource
    Increased intraepidermal CGRP correlates with local immuno-suppression after repeated broadband and narrowband UVB (2004)
    Oxford, UK; Malden, USA : Blackwell Publishing Ltd/Inc
    Experimental dermatology 13 (2004), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We investigated the effects of repeated broadband UVB (UVB-BB) and repeated narrowband UVB (UVB-NB) on intraepidermal nerve fibers (ENF) immunoreactive (IR) for CGRP and on CHS to DNFB in hairless mice. Mice were exposed to equivalent subinflammatory UVB-BB (Kodacel-filtered FS20) or UVB-NB (TL01) 3× per week for 4 weeks. One, 3, or 7 days after the last UV exposure, the number of CGRP-IR ENF was determined in exposed back skin. At the same time points, other mice were sensitized to DNFB on exposed back skin, challenged on abdominal skin 5 days later, and skin swelling was determined at 24 h after challenge. UVB-BB and UVB-NB significantly increased the number of CGRP-IR ENF in exposed back skin and significantly suppressed the sensitization of animals to DNFB. For both treatments, these effects were maximal 1 day after the last UV exposure. However, at 7 days after the last UV exposure, in UVB-NB-irradiated animals, the number of CGRP-IR ENF was still significantly increased and the sensitization to DNFB significantly suppressed, while in UVB-BB-irradiated animals, these parameters were similar to that in non-irradiated controls. Thus, while repeated exposure to UVB-BB or UVB-NB or both induced increase of CGRP-IR ENF as well as local immunosuppression, the effects after repeated UVB-NB were prolonged compared with that after repeated UVB-BB. This may contribute to the higher phototherapeutic efficacy of UVB-NB vs. UVB-BB.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0906-6705.2004.0212bs.x
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  • 4
    Electronic Resource
    Electronic Resource
    Neural regulation of endothelial cell-mediated inflammation (2004)
    Oxford, UK; Malden, USA : Blackwell Publishing Ltd/Inc
    Experimental dermatology 13 (2004), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: There is much evidence that neurocutaneous interactions may play an important role in modulating a wide variety of biological processes in the skin including inflammation. Perhaps, the key cell type for directing inflammatory processes in the skin is the dermal microvascular endothelial cell (DMEC). All leukocyte trafficking during cutaneous inflammation is mediated by DMEC. This presentation will review various ways in which the cutaneous neurosensory system can modulate DMEC activities, and how this may lead to novel approaches in our understanding and treatment of inflammatory skin disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0906-6705.2004.0212ac.x
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  • 5
    Electronic Resource
    Electronic Resource
    Calcitonin gene-related peptide and adrenomedullin modulate cytokine-induced microvascular endothelial cell cellular adhesion molecule expression and NF-κB activation (2004)
    Oxford, UK; Malden, USA : Blackwell Publishing Ltd/Inc
    Experimental dermatology 13 (2004), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: AM and the sensory neuropeptide CGRP are potent vasoactive mediators that activate high-affinity G-protein-coupled receptors consisting of receptor-activity modifying proteins (RAMPs) and a seven-transmembrane domain calcitonin receptor-like receptor (CRLR) with RAMP-1/CRLR as CGRP and RAMP2 or -3/CRLR as AM receptors. In this study, we have examined the possibility that AM or CGRP modulate dermal microvascular EC adhesion molecule (ICAM-1 and VCAM-1) expression. Primary HDMEC or cells of the EC line HMEC-1 were transfected with cDNA expression vectors for an EGFP control, RAMP-1, RAMP-2 and CRLR by electroporation, or left untransfected. Stimulation of EC-overexpressing R1/CRLR or R2/CRLR with CGRP or AM (0.01–1000 nm) resulted in a dose-dependent upregulation of intracellular cAMP. Importantly, when HDMEC transfected with R1/CRLR or R2/CRLR were treated with TNFα in combination with CGRP or AM, these peptides interfered with the TNF-induced expression of ICAM-1 and VCAM-1 as well as the adhesion of lymphoblastoid cell lines to HDMEC monolayer in a biphasic manner. Likewise, AM and CGRP modulated the activation of nuclear factor κB (NF-κB) partly by inhibiting the TNFα-induced degradation of cytosolic IκBα. Neither transfection with the orphan CRLR nor RAMPs alone was capable of mediating a full reduction of TNFα-induced ICAM-1 or VCAM-1 expression. In conclusion, CGRP and more pronounced AM are capable of modulating TNFα-induced EC CAM expression, which may be of importance for the regulation of leucocyte–endothelial cell interaction during cutaneous neurogenic inflammation.This study was supported by the “Medizinische Forschungsgesellschaft Salzburg” and a grant of the Austrian Science Foundation (P14906).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0906-6705.2004.0212bu.x
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  • 6
    Electronic Resource
    Electronic Resource
    Functional absence of neutral endopeptidase in mice promotes hapten uptake, maturation and function of bone marrow-derived dendritic cells (2004)
    Oxford, UK; Malden, USA : Blackwell Publishing Ltd/Inc
    Experimental dermatology 13 (2004), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The bioavailability of neuropeptides such as substance P (SP) released from sensory nerves or immune cells during skin inflammation is effectively controlled by proteolytic peptidases. Acute inhibition or genomic deletion of neutral endopeptidase (NEP) results in a SP-dependent augmentation of murine allergic contact dermatitis (ACD) by affecting sensitization and elicitation phase. In this study, we address the hypothesis that absence of NEP may modulate ACD responses by affecting bone marrow-derived dendritic cell (BmDC) maturation and function. BmDCs were generated from NEP-deficient mice (C57BL/6J-NEP–/–) or wild-type controls (C57BL/6J). FACS analysis revealed that d3, d6 and d7 NEP–/– BmDCs expressed significantly more DC cell-surface markers and costimulatory molecules compared to NEP+/+ mice BmDCs, in particular after BmDC maturation with LPS. In MLR utilizing d8 BmDCs pulsed 3 h in vitro with DNBS and T cells from in vivo DNFB-haptenized NEP–/– and NEP+/+ mice, BmDCs from NEP–/– animals promoted proliferation of T cells with higher efficacy compared to wild-type mice BmDCs. Likewise, T cells from NEP–/– mice demonstrated a higher proliferative response to Concavalin A stimulation or CD3/CD28 ligation compared to NEP+/+ mice. In addition, acute systemic NEP inhibition in NEP+/+ mice prior to sensitization with fluorescein isothiocyanate (FITC) after 24 h significantly augmented uptake of FITC in the CD11c-positive DC fraction from regional lymph nodes but not from spleen compared to cells obtained from mice not treated with the NEP inhibitor. These data indicate that functional absence of NEP may significantly control cutaneous ACD inflammatory responses by promoting hapten uptake, DC maturation and T-cell stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0906-6705.2004.0212bz.x
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  • 7
    Electronic Resource
    Electronic Resource
    Proteinase-activated receptor-2 in human skin: tissue distribution and activation of keratinocytes by mast cell tryptase (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Experimental dermatology 8 (1999), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Proteinase-activated receptor-2 (PAR-2) is a G-protein coupled receptor. Tryptic proteases cleave PAR-2 exposing a tethered ligand (SLIGKV), which binds and activates the receptor. Although PAR-2 is highy expressed by cultured keratinocytes and is an inflammatory mediator, its precise localization in the normal and inflamed human skin in unknown, and the proteases that activate PAR-2 in the skin have not been identified. We localized PAR-2 in human skin by immunohistochemistry, examined PAR-2 expression by RT-PCR and RNA blotting, and investigated PAR-2 activation by mast cell tryptase. PAR-2 was localized to keratinocytes, especially in the granular layer, to endothelial cells, hair follicles, myoepithelial cells of sweat glands, and dermal dendritic-like cells. PAR-2 was also highly expressed in keratinocytes and endothelial cells of inflamed skin. PAR-2 mRNA was detected in normal human skin by RT-PCR, and in cultured human keratinocytes and dermal microvascular endothelial cells by Northern hybridization. Trypsin, tryptase and a peptide corresponding to the tethered ligand (SLIGKVNG2) increased [Ca2+]i in keratinocytes, measured using Fura-2/AM. Although tryptase-containing mast cells were sparsely scattered in the normal dermis, they were numerous in the dermis in atopic dermatitis, and in the dermis, dermal-epidermal border, and occasionally within the lower epidermis in psoriasis. Tryptase may activate PAR-2 on keratinocytes and endothelial cells during inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0625.1999.tb00383.x
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  • 8
    Electronic Resource
    Electronic Resource
    Neuropeptides in the skin: interactions between the neuroendocrine and the skin immune systems (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Experimental dermatology 7 (1998), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The interaction between components of the nervous system and multiple target cells in the cutaneous immune system has been receiving increasing attention. It has been observed that certain skin diseases such as psoriasis and atopic dermatitis have a neurogenic component. Neuropeptides released by sensory nerves that innervate the skin and often contact epidermal and dermal cells can directly modulate functions of keratinocytes, Langerhans cells (LC), mast cells, dermal microvascular endothelial cells and infiltrating immune cells. Among these neuropeptides the tachykinins substance P (SP) and neurokinin A (NKA), calcitonin gene related peptide (CGRP), vasoactive intestinal peptide (VIP) and somato statin (SOM) have been reported to effectively modulate skin and immune cell functions such as cell proliferation, cytokine production or antigen presentation under physiological or pathophysiological conditions. Expression and regulation of their corresponding receptors that are expressed on a variety of skin cells as well as the presence of neuropeptidespecific peptidases such as neutral endopeptidase (NEP) or angiotensinconverting enzyme (ACE) determine the final biological response mediated by these peptides on the target cell or tissue. Likewise, skin cells like keratinocytes or fibroblasts are a source for neurotrophins such as nerve growth factor that are required not only for survival and regeneration of sensory neurons but also to control responsiveness of these neurons to external stimuli. Therefore, neuropeptides, neuropeptide receptors, neuropeptidedegrading enzymes and neurotrophins participate in a complex, interdependent network of mediators that modulate skin inflammation, wound healing and the skin immune system. This review will focus on recent studies demonstrating the role of tachykinins, CGRP, SOM and VIP and their receptors and neuropeptide-degrading enzymes in mediating neurogenic inflammation in the skin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0625.1998.tb00307.x
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