Functional absence of neutral endopeptidase in mice promotes hapten uptake, maturation and function of bone marrow‐derived dendritic cells
Identifieur interne : 000C74 ( Istex/Corpus ); précédent : 000C73; suivant : 000C75Functional absence of neutral endopeptidase in mice promotes hapten uptake, maturation and function of bone marrow‐derived dendritic cells
Auteurs : T. E. Scholzen ; M. Fastrich ; T. Brzoska ; C. A. Armstrong ; J. C. Ansel ; T. A. LugerSource :
- Experimental Dermatology [ 0906-6705 ] ; 2004-09.
English descriptors
- Teeft :
- 2department, 3department, Acth, Activates, Adhesion, Adrenomedullin, Agonist, Allergic dermatitis, Anagen, Antimicrobial, Antioxidant, Apoptosis, Apoptotic, Atopic, Atopic dermatitis, Autoimmune, Basal, Bdnf, Biomedical, Biomedical sciences, Bmdcs, Bohm1, Boltzmann, Calcitonin, Calcitonin peptide, Capsaicin, Cell biology, Cgrp, Charite, Costimulatory molecules, Cutaneous, Cutaneous inflammation, Cytokine, Cytotoxicity, Dendricity, Dendritic, Dendritic cells, Dermal, Dermal microvascular, Dermatitis, Dermatology, Endocrine, Endogenous, Endothelial, Endothelial cells, Eosinophil, Epidermal, Epithelial, Extracellular, Fibre, Fibroblast, Follicle, Functional role, Glutamine, Hacat, Hacat cells, Hair follicle, Hair follicles, Hair growth, Hamburg, Hdmec, Healthy subjects, Homeostasis, Human hair follicle, Human sebocytes, Human skin, Hyperalgesia, Immune, Immune cells, Immune response, Immune system, Immunobiology, Immunohistochemistry, Immunomodulatory, Immunoreactivity, Important role, Inflammation, Inflammatory, Insr, Internal medicine, Intracellular, Intracellular calcium concentration, Keratinocyte, Keratinocytes, Kinase, Ligand, Ludwig boltzmann institute, Luger1, Lymphocyte, Mast cells, Mc1r, Mediator, Melanin, Melanocortin, Melanocortin receptors, Melanocyte, Melanogenesis, Melanoma, Melanoma cells, Melatonin, Microvascular, Mitf, Modulators, Mrna, Msc, Munster, Murine, Naltrexone, Nerve fibers, Nerve fibres, Nerve growth factor, Nervous system, Neuroendocrine, Neurogenic, Neurogenic inflammation, Neuron, Neuropeptide, Neuropeptides, Neurotrophic, Neurotrophic factor, Neurotrophin, Neurotrophins, Neutral endopeptidase, Nk1r, Nmda, Pacap, Papilla, Par2, Pathway, Peptide, Peripheral blood eosinophils, Pigmentation, Plasma membrane, Pomc, Pomc peptides, Present study, Proinflammatory, Pruritus, Receptor, Regulator, Rheumatoid arthritis, Schwann, Sebaceous, Sebaceous gland, Sebocytes, Sensitization, Sensory nerves, Sensory neurons, Somatostatin, Trafficking, Transgenic, Transgenic mice, Trpv1, Tumour, Upregulated, Upregulation, Uremic pruritus, Urocortin, Vanilloid, Vasoactive, Vellus hair follicles, Wound healing.
Abstract
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.
Url:
DOI: 10.1111/j.0906-6705.2004.0212bz.x
Links to Exploration step
ISTEX:7974D9CBC6409957AE5CF67B9AF3F1FE9CDF6689Le document en format XML
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E." last="Scholzen">T. E. Scholzen</name><affiliation><mods:affiliation>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</mods:affiliation></affiliation></author><author><name sortKey="Fastrich, M" sort="Fastrich, M" uniqKey="Fastrich M" first="M." last="Fastrich">M. Fastrich</name><affiliation><mods:affiliation>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</mods:affiliation></affiliation></author><author><name sortKey="Brzoska, T" sort="Brzoska, T" uniqKey="Brzoska T" first="T." last="Brzoska">T. Brzoska</name><affiliation><mods:affiliation>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</mods:affiliation></affiliation></author><author><name sortKey="Armstrong, C A" sort="Armstrong, C A" uniqKey="Armstrong C" first="C. A." last="Armstrong">C. A. Armstrong</name><affiliation><mods:affiliation>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</mods:affiliation></affiliation></author><author><name sortKey="Ansel, J C" sort="Ansel, J C" uniqKey="Ansel J" first="J. C." last="Ansel">J. C. 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Luger</name><affiliation><mods:affiliation>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Experimental Dermatology</title><idno type="ISSN">0906-6705</idno><idno type="eISSN">1600-0625</idno><imprint><publisher>Blackwell Publishing Ltd/Inc</publisher><pubPlace>Oxford, UK; Malden, USA</pubPlace><date type="published" when="2004-09">2004-09</date><biblScope unit="volume">13</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="587">587</biblScope><biblScope unit="page" to="587">587</biblScope></imprint><idno type="ISSN">0906-6705</idno></series><idno type="istex">7974D9CBC6409957AE5CF67B9AF3F1FE9CDF6689</idno><idno type="DOI">10.1111/j.0906-6705.2004.0212bz.x</idno><idno type="ArticleID">EXD212BZ</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0906-6705</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>2department</term><term>3department</term><term>Acth</term><term>Activates</term><term>Adhesion</term><term>Adrenomedullin</term><term>Agonist</term><term>Allergic dermatitis</term><term>Anagen</term><term>Antimicrobial</term><term>Antioxidant</term><term>Apoptosis</term><term>Apoptotic</term><term>Atopic</term><term>Atopic dermatitis</term><term>Autoimmune</term><term>Basal</term><term>Bdnf</term><term>Biomedical</term><term>Biomedical sciences</term><term>Bmdcs</term><term>Bohm1</term><term>Boltzmann</term><term>Calcitonin</term><term>Calcitonin peptide</term><term>Capsaicin</term><term>Cell biology</term><term>Cgrp</term><term>Charite</term><term>Costimulatory molecules</term><term>Cutaneous</term><term>Cutaneous inflammation</term><term>Cytokine</term><term>Cytotoxicity</term><term>Dendricity</term><term>Dendritic</term><term>Dendritic cells</term><term>Dermal</term><term>Dermal microvascular</term><term>Dermatitis</term><term>Dermatology</term><term>Endocrine</term><term>Endogenous</term><term>Endothelial</term><term>Endothelial cells</term><term>Eosinophil</term><term>Epidermal</term><term>Epithelial</term><term>Extracellular</term><term>Fibre</term><term>Fibroblast</term><term>Follicle</term><term>Functional role</term><term>Glutamine</term><term>Hacat</term><term>Hacat cells</term><term>Hair follicle</term><term>Hair follicles</term><term>Hair growth</term><term>Hamburg</term><term>Hdmec</term><term>Healthy subjects</term><term>Homeostasis</term><term>Human hair follicle</term><term>Human sebocytes</term><term>Human skin</term><term>Hyperalgesia</term><term>Immune</term><term>Immune cells</term><term>Immune response</term><term>Immune system</term><term>Immunobiology</term><term>Immunohistochemistry</term><term>Immunomodulatory</term><term>Immunoreactivity</term><term>Important role</term><term>Inflammation</term><term>Inflammatory</term><term>Insr</term><term>Internal medicine</term><term>Intracellular</term><term>Intracellular calcium concentration</term><term>Keratinocyte</term><term>Keratinocytes</term><term>Kinase</term><term>Ligand</term><term>Ludwig boltzmann institute</term><term>Luger1</term><term>Lymphocyte</term><term>Mast cells</term><term>Mc1r</term><term>Mediator</term><term>Melanin</term><term>Melanocortin</term><term>Melanocortin receptors</term><term>Melanocyte</term><term>Melanogenesis</term><term>Melanoma</term><term>Melanoma cells</term><term>Melatonin</term><term>Microvascular</term><term>Mitf</term><term>Modulators</term><term>Mrna</term><term>Msc</term><term>Munster</term><term>Murine</term><term>Naltrexone</term><term>Nerve fibers</term><term>Nerve fibres</term><term>Nerve growth factor</term><term>Nervous system</term><term>Neuroendocrine</term><term>Neurogenic</term><term>Neurogenic inflammation</term><term>Neuron</term><term>Neuropeptide</term><term>Neuropeptides</term><term>Neurotrophic</term><term>Neurotrophic factor</term><term>Neurotrophin</term><term>Neurotrophins</term><term>Neutral endopeptidase</term><term>Nk1r</term><term>Nmda</term><term>Pacap</term><term>Papilla</term><term>Par2</term><term>Pathway</term><term>Peptide</term><term>Peripheral blood eosinophils</term><term>Pigmentation</term><term>Plasma membrane</term><term>Pomc</term><term>Pomc peptides</term><term>Present study</term><term>Proinflammatory</term><term>Pruritus</term><term>Receptor</term><term>Regulator</term><term>Rheumatoid arthritis</term><term>Schwann</term><term>Sebaceous</term><term>Sebaceous gland</term><term>Sebocytes</term><term>Sensitization</term><term>Sensory nerves</term><term>Sensory neurons</term><term>Somatostatin</term><term>Trafficking</term><term>Transgenic</term><term>Transgenic mice</term><term>Trpv1</term><term>Tumour</term><term>Upregulated</term><term>Upregulation</term><term>Uremic pruritus</term><term>Urocortin</term><term>Vanilloid</term><term>Vasoactive</term><term>Vellus hair follicles</term><term>Wound healing</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>receptor</json:string><json:string>dermatology</json:string><json:string>follicle</json:string><json:string>keratinocytes</json:string><json:string>cutaneous</json:string><json:string>melanocyte</json:string><json:string>fibroblast</json:string><json:string>peptide</json:string><json:string>munster</json:string><json:string>mc1r</json:string><json:string>immune</json:string><json:string>pathway</json:string><json:string>inflammation</json:string><json:string>neuropeptides</json:string><json:string>melanoma</json:string><json:string>cgrp</json:string><json:string>epidermal</json:string><json:string>neurogenic</json:string><json:string>pomc</json:string><json:string>agonist</json:string><json:string>bdnf</json:string><json:string>dermatitis</json:string><json:string>2department</json:string><json:string>neuropeptide</json:string><json:string>dermal</json:string><json:string>capsaicin</json:string><json:string>pruritus</json:string><json:string>fibre</json:string><json:string>human 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follicle</json:string><json:string>sebaceous</json:string><json:string>pomc peptides</json:string><json:string>cell biology</json:string><json:string>melanin</json:string><json:string>neurotrophin</json:string><json:string>par2</json:string><json:string>melanogenesis</json:string><json:string>upregulated</json:string><json:string>nmda</json:string><json:string>hacat cells</json:string><json:string>papilla</json:string><json:string>pacap</json:string><json:string>immunoreactivity</json:string><json:string>sensory neurons</json:string><json:string>sensory nerves</json:string><json:string>cytotoxicity</json:string><json:string>naltrexone</json:string><json:string>msc</json:string><json:string>basal</json:string><json:string>schwann</json:string><json:string>immunobiology</json:string><json:string>anagen</json:string><json:string>antimicrobial</json:string><json:string>antioxidant</json:string><json:string>trafficking</json:string><json:string>calcitonin 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E. Scholzen</name><affiliations><json:string>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</json:string></affiliations></json:item><json:item><name>M. Fastrich</name><affiliations><json:string>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</json:string></affiliations></json:item><json:item><name>T. Brzoska</name><affiliations><json:string>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</json:string></affiliations></json:item><json:item><name>C. A. Armstrong</name><affiliations><json:string>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</json:string></affiliations></json:item><json:item><name>J. C. Ansel</name><affiliations><json:string>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</json:string></affiliations></json:item><json:item><name>T. A. Luger</name><affiliations><json:string>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</json:string></affiliations></json:item></author><articleId><json:string>EXD212BZ</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>abstract</json:string></originalGenre><abstract>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.</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595 x 782 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractCharCount>1756</abstractCharCount><pdfWordCount>23570</pdfWordCount><pdfCharCount>158516</pdfCharCount><pdfPageCount>25</pdfPageCount><abstractWordCount>251</abstractWordCount></qualityIndicators><title>Functional absence of neutral endopeptidase in mice promotes hapten uptake, maturation and function of bone marrow‐derived dendritic cells</title><genre><json:string>abstract</json:string></genre><host><title>Experimental Dermatology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1600-0625</json:string></doi><issn><json:string>0906-6705</json:string></issn><eissn><json:string>1600-0625</json:string></eissn><publisherId><json:string>EXD</json:string></publisherId><volume>13</volume><issue>9</issue><pages><first>587</first><last>587</last><total>1</total></pages><genre><json:string>journal</json:string></genre></host><categories><wos><json:string>science</json:string><json:string>dermatology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>dermatology & venereal diseases</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string></inist></categories><publicationDate>2004</publicationDate><copyrightDate>2004</copyrightDate><doi><json:string>10.1111/j.0906-6705.2004.0212bz.x</json:string></doi><id>7974D9CBC6409957AE5CF67B9AF3F1FE9CDF6689</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/7974D9CBC6409957AE5CF67B9AF3F1FE9CDF6689/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/7974D9CBC6409957AE5CF67B9AF3F1FE9CDF6689/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/7974D9CBC6409957AE5CF67B9AF3F1FE9CDF6689/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Functional absence of neutral endopeptidase in mice promotes hapten uptake, maturation and function of bone marrow‐derived dendritic cells</title><respStmt><resp>Références bibliographiques récupérées via GROBID</resp><name resp="ISTEX-API">ISTEX-API (INIST-CNRS)</name></respStmt><respStmt><resp>Références bibliographiques récupérées via GROBID</resp><name resp="ISTEX-API">ISTEX-API (INIST-CNRS)</name></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd/Inc</publisher><pubPlace>Oxford, UK; Malden, USA</pubPlace><availability><p>WILEY</p></availability><date>2004</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Functional absence of neutral endopeptidase in mice promotes hapten uptake, maturation and function of bone marrow‐derived dendritic cells</title><author xml:id="author-1"><persName><forename type="first">T. E.</forename><surname>Scholzen</surname></persName><affiliation>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</affiliation></author><author xml:id="author-2"><persName><forename type="first">M.</forename><surname>Fastrich</surname></persName><affiliation>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</affiliation></author><author xml:id="author-3"><persName><forename type="first">T.</forename><surname>Brzoska</surname></persName><affiliation>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</affiliation></author><author xml:id="author-4"><persName><forename type="first">C. A.</forename><surname>Armstrong</surname></persName><affiliation>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</affiliation></author><author xml:id="author-5"><persName><forename type="first">J. C.</forename><surname>Ansel</surname></persName><affiliation>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</affiliation></author><author xml:id="author-6"><persName><forename type="first">T. A.</forename><surname>Luger</surname></persName><affiliation>1 Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and 2 Department of Dermatology, Northwestern University, Chicago, IL, USA</affiliation></author></analytic><monogr><title level="j">Experimental Dermatology</title><idno type="pISSN">0906-6705</idno><idno type="eISSN">1600-0625</idno><idno type="DOI">10.1111/(ISSN)1600-0625</idno><imprint><publisher>Blackwell Publishing Ltd/Inc</publisher><pubPlace>Oxford, UK; Malden, USA</pubPlace><date type="published" when="2004-09"></date><biblScope unit="volume">13</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="587">587</biblScope><biblScope unit="page" to="587">587</biblScope></imprint></monogr><idno type="istex">7974D9CBC6409957AE5CF67B9AF3F1FE9CDF6689</idno><idno type="DOI">10.1111/j.0906-6705.2004.0212bz.x</idno><idno type="ArticleID">EXD212BZ</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2004</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>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. 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E.</givenNames><familyName>Scholzen</familyName></personName></creator> 1 <creator creatorRole="author" xml:id="cr2" affiliationRef="#aff-1-1"><personName><givenNames>M.</givenNames><familyName>Fastrich</familyName></personName></creator> 1 <creator creatorRole="author" xml:id="cr3" affiliationRef="#aff-1-1"><personName><givenNames>T.</givenNames><familyName>Brzoska</familyName></personName></creator> 1 <creator creatorRole="author" xml:id="cr4" affiliationRef="#aff-1-1"><personName><givenNames>C. A.</givenNames><familyName>Armstrong</familyName></personName></creator> 2 <creator creatorRole="author" xml:id="cr5" affiliationRef="#aff-1-1"><personName><givenNames>J. C.</givenNames><familyName>Ansel</familyName></personName></creator> 2 <creator creatorRole="author" xml:id="cr6" affiliationRef="#aff-1-1"><personName><givenNames>T. A.</givenNames><familyName>Luger</familyName></personName></creator> 1 </creators><affiliationGroup><affiliation xml:id="aff-1-1" countryCode="US"><unparsedAffiliation><b><sup>1</sup> Ludwig‐Boltzmann Institute, Department of Dermatology, University of Münster, Münster, Germany, and <sup>2</sup> Department of Dermatology, Northwestern University, Chicago, IL, USA </b></unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><p>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<sup>–/–</sup>) or wild‐type controls (C57BL/6J). FACS analysis revealed that d3, d6 and d7 NEP<sup>–/–</sup> BmDCs expressed significantly more DC cell‐surface markers and costimulatory molecules compared to NEP<sup>+/+</sup> mice BmDCs, in particular after BmDC maturation with LPS. In MLR utilizing d8 BmDCs pulsed 3 h <i>in vitro</i> with DNBS and T cells from <i>in vivo</i> DNFB‐haptenized NEP<sup>–/–</sup> and NEP<sup>+/+</sup> mice, BmDCs from NEP<sup>–/–</sup> animals promoted proliferation of T cells with higher efficacy compared to wild‐type mice BmDCs. Likewise, T cells from NEP<sup>–/–</sup> mice demonstrated a higher proliferative response to Concavalin A stimulation or CD3/CD28 ligation compared to NEP<sup>+/+</sup> mice. In addition, acute systemic NEP inhibition in NEP<sup>+/+</sup> 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. 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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. 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