Increased nerve growth factor and its receptors in atopic dermatitis : an immunohistochemical study
Evidence suggests that neurotrophins may regulate certain immune functions and inflammation. In the present study, the localization and distribution of nerve growth factor (NGF) and its receptors were explored using immunohistochemical methods, with the aim of detecting the cause of the neurohyperpl...
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description | Evidence suggests that neurotrophins may regulate certain immune functions and inflammation. In the present study, the localization and distribution of nerve growth factor (NGF) and its receptors were explored using immunohistochemical methods, with the aim of detecting the cause of the neurohyperplasia in early lesions of atopic dermatitis (AD). In AD involved skin, strong NGF-immunoreactive (IR) cells were observed in the epidermis. In some cases, a huge number of infiltrating cells with stronger NGF immunoreactivity was seen mainly in the dermal papillae. Some trkA immunoreactivity was observed in the outer membrane of cells in the basal and spinal layers of the epidermis. In the papillary dermis, a larger number of cells demonstrated strong trkA immunoreactivity. The p75 NGFr-IR nerve fibre profiles were increased (900 per mm(2); p |
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In the present study, the localization and distribution of nerve growth factor (NGF) and its receptors were explored using immunohistochemical methods, with the aim of detecting the cause of the neurohyperplasia in early lesions of atopic dermatitis (AD). In AD involved skin, strong NGF-immunoreactive (IR) cells were observed in the epidermis. In some cases, a huge number of infiltrating cells with stronger NGF immunoreactivity was seen mainly in the dermal papillae. Some trkA immunoreactivity was observed in the outer membrane of cells in the basal and spinal layers of the epidermis. In the papillary dermis, a larger number of cells demonstrated strong trkA immunoreactivity. The p75 NGFr-IR nerve fibre profiles were increased (900 per mm(2); p<0.001) compared to normal [the involved skin also differed from the uninvolved skin (p<0.05)] in the dermal papillae. These nerve fibres were larger, coarser and branched, some of them terminated at p75 NGFr-IR basal cells, and also revealed a stronger fluorescence staining than the controls or the uninvolved skin. In normal healthy volunteers and AD uninvolved skin, the NGF immunoreactivity was weak in the basal layer of epidermis. Only a few trkA positive cells were seen in the basal layer of the epidermis and upper dermis. The IR epidermal basal cells revealed a striking patchy arrangement with strong p75 NGFr immunostaining in the peripheral part of the cells, and short and thick NGFr-IR nerve fibre profiles appeared as smooth endings scattered in the dermis including the cutaneous accessory organs. Using NGF and p75 NGFr double staining, both immunoreactivities showed a weak staining in the epidermis and dermis in normal and uninvolved skin. In the involved dermis of AD, the intensity of p75 NGFr-IR nerves was stronger in areas where there were also increased numbers of NGF-IR cells. These findings indicate that NGF and its receptors may contribute to the neurohyperplasia of AD.</description><identifier>ISSN: 0340-3696</identifier><identifier>EISSN: 1432-069X</identifier><identifier>DOI: 10.1007/s00403-006-0657-1</identifier><identifier>PMID: 16586073</identifier><identifier>CODEN: ADREDL</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Adult ; Allergic diseases ; Biological and medical sciences ; Case-Control Studies ; Dermatitis, Atopic - metabolism ; Dermatitis, Atopic - pathology ; Dermatology ; Dermis - metabolism ; Dermis - pathology ; Humans ; Immunopathology ; Medical sciences ; Medicin och hälsovetenskap ; Middle Aged ; Nerve Fibers - metabolism ; Nerve Fibers - pathology ; Nerve Growth Factor - metabolism ; Receptor, Nerve Growth Factor - metabolism ; Receptor, trkA - metabolism ; Receptors, Nerve Growth Factor - metabolism ; Skin allergic diseases. 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In the present study, the localization and distribution of nerve growth factor (NGF) and its receptors were explored using immunohistochemical methods, with the aim of detecting the cause of the neurohyperplasia in early lesions of atopic dermatitis (AD). In AD involved skin, strong NGF-immunoreactive (IR) cells were observed in the epidermis. In some cases, a huge number of infiltrating cells with stronger NGF immunoreactivity was seen mainly in the dermal papillae. Some trkA immunoreactivity was observed in the outer membrane of cells in the basal and spinal layers of the epidermis. In the papillary dermis, a larger number of cells demonstrated strong trkA immunoreactivity. The p75 NGFr-IR nerve fibre profiles were increased (900 per mm(2); p<0.001) compared to normal [the involved skin also differed from the uninvolved skin (p<0.05)] in the dermal papillae. These nerve fibres were larger, coarser and branched, some of them terminated at p75 NGFr-IR basal cells, and also revealed a stronger fluorescence staining than the controls or the uninvolved skin. In normal healthy volunteers and AD uninvolved skin, the NGF immunoreactivity was weak in the basal layer of epidermis. Only a few trkA positive cells were seen in the basal layer of the epidermis and upper dermis. The IR epidermal basal cells revealed a striking patchy arrangement with strong p75 NGFr immunostaining in the peripheral part of the cells, and short and thick NGFr-IR nerve fibre profiles appeared as smooth endings scattered in the dermis including the cutaneous accessory organs. Using NGF and p75 NGFr double staining, both immunoreactivities showed a weak staining in the epidermis and dermis in normal and uninvolved skin. In the involved dermis of AD, the intensity of p75 NGFr-IR nerves was stronger in areas where there were also increased numbers of NGF-IR cells. These findings indicate that NGF and its receptors may contribute to the neurohyperplasia of AD.</description><subject>Adult</subject><subject>Allergic diseases</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Dermatitis, Atopic - metabolism</subject><subject>Dermatitis, Atopic - pathology</subject><subject>Dermatology</subject><subject>Dermis - metabolism</subject><subject>Dermis - pathology</subject><subject>Humans</subject><subject>Immunopathology</subject><subject>Medical sciences</subject><subject>Medicin och hälsovetenskap</subject><subject>Middle Aged</subject><subject>Nerve Fibers - metabolism</subject><subject>Nerve Fibers - pathology</subject><subject>Nerve Growth Factor - metabolism</subject><subject>Receptor, Nerve Growth Factor - metabolism</subject><subject>Receptor, trkA - metabolism</subject><subject>Receptors, Nerve Growth Factor - metabolism</subject><subject>Skin allergic diseases. Stinging insect allergies</subject><issn>0340-3696</issn><issn>1432-069X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kVFrFDEQx4Mo9qj9AL5IEPRtdZJsko1vUrQtFHxR8C1ks7Ne6u3mTLIt_fbmuNUDwbxkMvx-w5A_IS8ZvGMA-n0GaEE0AKoBJXXDnpANawWvL_P9KdmAaKERyqgzcpHzHdSjoeWgn5MzpmSnQIsN8TezT-gyDnTGdI_0R4oPZUtH50tM1M0DDSXThB73tZFpmKkrcR88HTBNroQSMv1QQRqmaZnjNuQS_Ran4N2O5rIMjy_Is9HtMl6s9zn59vnT18vr5vbL1c3lx9vGSyFKg7JH6fVgmDIt1AIGkL3QTBopQPhReWV6w53AnmvFjXOddlwIlN3Y8Vack-Y4Nz_gfuntPoXJpUcbXbBr62et0EqtWGcqr__L71McTtIfkZnWaMOr-fZoVuzXgrnYKWSPu52bMS7ZKm2k6jpZwdf_gHdxSXP9BcsZ5yAkYxViR8inmHPC8e8mDOwha3vM2tas7SFre3BerYOXfsLhZKzJVuDNCrhckxiTm33IJ07rThrVid-ZMrLW</recordid><startdate>20060601</startdate><enddate>20060601</enddate><creator>DOU, Ying-Chun</creator><creator>HAGSTRÖMER, Lena</creator><creator>EMTESTAM, Lennart</creator><creator>JOHANSSON, Olle</creator><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>20060601</creationdate><title>Increased nerve growth factor and its receptors in atopic dermatitis : an immunohistochemical study</title><author>DOU, Ying-Chun ; HAGSTRÖMER, Lena ; EMTESTAM, Lennart ; JOHANSSON, Olle</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c533t-e5be5c7d916940c7d0d05b371595303cf6c69b92a3eb27629aa87a233e58f8243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adult</topic><topic>Allergic diseases</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Dermatitis, Atopic - metabolism</topic><topic>Dermatitis, Atopic - pathology</topic><topic>Dermatology</topic><topic>Dermis - metabolism</topic><topic>Dermis - pathology</topic><topic>Humans</topic><topic>Immunopathology</topic><topic>Medical sciences</topic><topic>Medicin och hälsovetenskap</topic><topic>Middle Aged</topic><topic>Nerve Fibers - metabolism</topic><topic>Nerve Fibers - pathology</topic><topic>Nerve Growth Factor - metabolism</topic><topic>Receptor, Nerve Growth Factor - metabolism</topic><topic>Receptor, trkA - metabolism</topic><topic>Receptors, Nerve Growth Factor - metabolism</topic><topic>Skin allergic diseases. Stinging insect allergies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DOU, Ying-Chun</creatorcontrib><creatorcontrib>HAGSTRÖMER, Lena</creatorcontrib><creatorcontrib>EMTESTAM, Lennart</creatorcontrib><creatorcontrib>JOHANSSON, Olle</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>ARCHIVES OF DERMATOLOGICAL RESEARCH</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>DOU, Ying-Chun</au><au>HAGSTRÖMER, Lena</au><au>EMTESTAM, Lennart</au><au>JOHANSSON, Olle</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased nerve growth factor and its receptors in atopic dermatitis : an immunohistochemical study</atitle><jtitle>ARCHIVES OF DERMATOLOGICAL RESEARCH</jtitle><addtitle>Arch Dermatol Res</addtitle><date>2006-06-01</date><risdate>2006</risdate><volume>298</volume><issue>1</issue><spage>31</spage><epage>37</epage><pages>31-37</pages><issn>0340-3696</issn><eissn>1432-069X</eissn><coden>ADREDL</coden><abstract>Evidence suggests that neurotrophins may regulate certain immune functions and inflammation. In the present study, the localization and distribution of nerve growth factor (NGF) and its receptors were explored using immunohistochemical methods, with the aim of detecting the cause of the neurohyperplasia in early lesions of atopic dermatitis (AD). In AD involved skin, strong NGF-immunoreactive (IR) cells were observed in the epidermis. In some cases, a huge number of infiltrating cells with stronger NGF immunoreactivity was seen mainly in the dermal papillae. Some trkA immunoreactivity was observed in the outer membrane of cells in the basal and spinal layers of the epidermis. In the papillary dermis, a larger number of cells demonstrated strong trkA immunoreactivity. The p75 NGFr-IR nerve fibre profiles were increased (900 per mm(2); p<0.001) compared to normal [the involved skin also differed from the uninvolved skin (p<0.05)] in the dermal papillae. These nerve fibres were larger, coarser and branched, some of them terminated at p75 NGFr-IR basal cells, and also revealed a stronger fluorescence staining than the controls or the uninvolved skin. In normal healthy volunteers and AD uninvolved skin, the NGF immunoreactivity was weak in the basal layer of epidermis. Only a few trkA positive cells were seen in the basal layer of the epidermis and upper dermis. The IR epidermal basal cells revealed a striking patchy arrangement with strong p75 NGFr immunostaining in the peripheral part of the cells, and short and thick NGFr-IR nerve fibre profiles appeared as smooth endings scattered in the dermis including the cutaneous accessory organs. Using NGF and p75 NGFr double staining, both immunoreactivities showed a weak staining in the epidermis and dermis in normal and uninvolved skin. In the involved dermis of AD, the intensity of p75 NGFr-IR nerves was stronger in areas where there were also increased numbers of NGF-IR cells. These findings indicate that NGF and its receptors may contribute to the neurohyperplasia of AD.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>16586073</pmid><doi>10.1007/s00403-006-0657-1</doi><tpages>7</tpages></addata></record> |
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subjects | Adult Allergic diseases Biological and medical sciences Case-Control Studies Dermatitis, Atopic - metabolism Dermatitis, Atopic - pathology Dermatology Dermis - metabolism Dermis - pathology Humans Immunopathology Medical sciences Medicin och hälsovetenskap Middle Aged Nerve Fibers - metabolism Nerve Fibers - pathology Nerve Growth Factor - metabolism Receptor, Nerve Growth Factor - metabolism Receptor, trkA - metabolism Receptors, Nerve Growth Factor - metabolism Skin allergic diseases. Stinging insect allergies |
title | Increased nerve growth factor and its receptors in atopic dermatitis : an immunohistochemical study |
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