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The participation of proliferative keratinocytes in the preimmune response to sensitizing agents
The aims of this study were to investigate whether keratinocytes are capable of playing a direct preimmune role in the pathophysiology of allergic contact dermatitis (ACD) and to examine to what extent the degree of differentiation might influence this. We measured the ability of sensitizing agents...
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| Published in: | British journal of dermatology (1951) 1998-01, Vol.138 (1), p.45-56 |
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| container_title | British journal of dermatology (1951) |
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| creator | LITTLE, M. C METCALFE, R. A HAYCOCK, J. W HEALY, J GAWKRODGER, D. J NEIL, S. M |
| description | The aims of this study were to investigate whether keratinocytes are capable of playing a direct preimmune role in the pathophysiology of allergic contact dermatitis (ACD) and to examine to what extent the degree of differentiation might influence this. We measured the ability of sensitizing agents to up‐regulate intercellular adhesion molecule 1 (ICAM‐1) expression in cultured normal human keratinocytes (NHK) and in the transformed human keratinocyte HaCaT cell line. In proliferative HaCaT cells, following a 24 h exposure, nickel compounds, para‐phenylenediamine (pPD) and 1‐chloro‐2,4‐dinitrobenzene produced a concentration‐dependent up‐regulation of ICAM‐1 expression without reducing cell viability, while K2Cr2O7 led to ICAM‐1 up‐regulation at cytotoxic concentrations, and CrCl3 was without effect. In NHK, NiSO4 and pPD induced ICAM‐1 expression to a significantly greater extent in proliferative cells than in differentiated cells, where involucrin expression was measured to assess the differentiation state. NiSO4‐ or pPD‐pretreatment of proliferative HaCaT cells enhanced T‐cell binding, which was abolished by neutralizing antibodies to ICAM‐1 or CD18. Our investigations concerning the involvement of oxidative stress in the induction of ICAM‐1 expression in response to sensitizing agents were inconclusive. The oxidizing agents FeCl3 and H2O2 up‐regulated ICAM‐1 expression in HaCaT cells but there was no clear relationship between the ability of agents to induce ICAM‐1 expression and their ability to alter the levels of reduced glutathione. Although pPD increased interleukin‐1α release from NHK, this cytokine was not capable of inducing ICAM‐1 expression in NHK. Tumour necrosis factor‐α, which does induce ICAM‐1 expression in NHK, was not detected in response to pPD, arguing against an autocrine pathway of ICAM‐1 induction in response to pPD. In summary, we report the direct interaction of sensitizing agents with keratinocytes leading to the generation of immune signals, particularly by proliferative keratinocytes, suggesting an active role for the proliferative keratinocyte in the pathophysiology of ACD. |
| doi_str_mv | 10.1046/j.1365-2133.1998.02025.x |
| format | article |
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C ; METCALFE, R. A ; HAYCOCK, J. W ; HEALY, J ; GAWKRODGER, D. J ; NEIL, S. M</creator><creatorcontrib>LITTLE, M. C ; METCALFE, R. A ; HAYCOCK, J. W ; HEALY, J ; GAWKRODGER, D. J ; NEIL, S. M</creatorcontrib><description>The aims of this study were to investigate whether keratinocytes are capable of playing a direct preimmune role in the pathophysiology of allergic contact dermatitis (ACD) and to examine to what extent the degree of differentiation might influence this. We measured the ability of sensitizing agents to up‐regulate intercellular adhesion molecule 1 (ICAM‐1) expression in cultured normal human keratinocytes (NHK) and in the transformed human keratinocyte HaCaT cell line. In proliferative HaCaT cells, following a 24 h exposure, nickel compounds, para‐phenylenediamine (pPD) and 1‐chloro‐2,4‐dinitrobenzene produced a concentration‐dependent up‐regulation of ICAM‐1 expression without reducing cell viability, while K2Cr2O7 led to ICAM‐1 up‐regulation at cytotoxic concentrations, and CrCl3 was without effect. In NHK, NiSO4 and pPD induced ICAM‐1 expression to a significantly greater extent in proliferative cells than in differentiated cells, where involucrin expression was measured to assess the differentiation state. NiSO4‐ or pPD‐pretreatment of proliferative HaCaT cells enhanced T‐cell binding, which was abolished by neutralizing antibodies to ICAM‐1 or CD18. Our investigations concerning the involvement of oxidative stress in the induction of ICAM‐1 expression in response to sensitizing agents were inconclusive. The oxidizing agents FeCl3 and H2O2 up‐regulated ICAM‐1 expression in HaCaT cells but there was no clear relationship between the ability of agents to induce ICAM‐1 expression and their ability to alter the levels of reduced glutathione. Although pPD increased interleukin‐1α release from NHK, this cytokine was not capable of inducing ICAM‐1 expression in NHK. Tumour necrosis factor‐α, which does induce ICAM‐1 expression in NHK, was not detected in response to pPD, arguing against an autocrine pathway of ICAM‐1 induction in response to pPD. In summary, we report the direct interaction of sensitizing agents with keratinocytes leading to the generation of immune signals, particularly by proliferative keratinocytes, suggesting an active role for the proliferative keratinocyte in the pathophysiology of ACD.</description><identifier>ISSN: 0007-0963</identifier><identifier>EISSN: 1365-2133</identifier><identifier>DOI: 10.1046/j.1365-2133.1998.02025.x</identifier><identifier>PMID: 9536222</identifier><identifier>CODEN: BJDEAZ</identifier><language>eng</language><publisher>Oxford BSL: Blackwell Science Ltd</publisher><subject>Allergens - immunology ; Allergic diseases ; Biological and medical sciences ; Cell Adhesion - immunology ; Cell Culture Techniques ; Cell Differentiation - immunology ; Cell Division - immunology ; Cell Line ; Cytokines - immunology ; Dermatitis, Allergic Contact - immunology ; Dermatitis, Allergic Contact - pathology ; Dose-Response Relationship, Immunologic ; Humans ; Immunopathology ; Intercellular Adhesion Molecule-1 - metabolism ; Keratinocytes - immunology ; Keratinocytes - pathology ; Medical sciences ; Oxidative Stress ; Skin allergic diseases. Stinging insect allergies ; T-Lymphocytes - immunology ; Up-Regulation - immunology</subject><ispartof>British journal of dermatology (1951), 1998-01, Vol.138 (1), p.45-56</ispartof><rights>British Association of Dermatology</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4315-3ae607f54907d1fc7329900086e4bf82f808c2e1fb65cd7a9d1237dfefc9c9f43</citedby><cites>FETCH-LOGICAL-c4315-3ae607f54907d1fc7329900086e4bf82f808c2e1fb65cd7a9d1237dfefc9c9f43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1365-2133.1998.02025.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1365-2133.1998.02025.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,786,790,4043,27956,27957,27958,50923,51032</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2133582$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9536222$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LITTLE, M. C</creatorcontrib><creatorcontrib>METCALFE, R. A</creatorcontrib><creatorcontrib>HAYCOCK, J. W</creatorcontrib><creatorcontrib>HEALY, J</creatorcontrib><creatorcontrib>GAWKRODGER, D. J</creatorcontrib><creatorcontrib>NEIL, S. M</creatorcontrib><title>The participation of proliferative keratinocytes in the preimmune response to sensitizing agents</title><title>British journal of dermatology (1951)</title><addtitle>British Journal of Dermatology</addtitle><description>The aims of this study were to investigate whether keratinocytes are capable of playing a direct preimmune role in the pathophysiology of allergic contact dermatitis (ACD) and to examine to what extent the degree of differentiation might influence this. We measured the ability of sensitizing agents to up‐regulate intercellular adhesion molecule 1 (ICAM‐1) expression in cultured normal human keratinocytes (NHK) and in the transformed human keratinocyte HaCaT cell line. In proliferative HaCaT cells, following a 24 h exposure, nickel compounds, para‐phenylenediamine (pPD) and 1‐chloro‐2,4‐dinitrobenzene produced a concentration‐dependent up‐regulation of ICAM‐1 expression without reducing cell viability, while K2Cr2O7 led to ICAM‐1 up‐regulation at cytotoxic concentrations, and CrCl3 was without effect. In NHK, NiSO4 and pPD induced ICAM‐1 expression to a significantly greater extent in proliferative cells than in differentiated cells, where involucrin expression was measured to assess the differentiation state. NiSO4‐ or pPD‐pretreatment of proliferative HaCaT cells enhanced T‐cell binding, which was abolished by neutralizing antibodies to ICAM‐1 or CD18. Our investigations concerning the involvement of oxidative stress in the induction of ICAM‐1 expression in response to sensitizing agents were inconclusive. The oxidizing agents FeCl3 and H2O2 up‐regulated ICAM‐1 expression in HaCaT cells but there was no clear relationship between the ability of agents to induce ICAM‐1 expression and their ability to alter the levels of reduced glutathione. Although pPD increased interleukin‐1α release from NHK, this cytokine was not capable of inducing ICAM‐1 expression in NHK. Tumour necrosis factor‐α, which does induce ICAM‐1 expression in NHK, was not detected in response to pPD, arguing against an autocrine pathway of ICAM‐1 induction in response to pPD. In summary, we report the direct interaction of sensitizing agents with keratinocytes leading to the generation of immune signals, particularly by proliferative keratinocytes, suggesting an active role for the proliferative keratinocyte in the pathophysiology of ACD.</description><subject>Allergens - immunology</subject><subject>Allergic diseases</subject><subject>Biological and medical sciences</subject><subject>Cell Adhesion - immunology</subject><subject>Cell Culture Techniques</subject><subject>Cell Differentiation - immunology</subject><subject>Cell Division - immunology</subject><subject>Cell Line</subject><subject>Cytokines - immunology</subject><subject>Dermatitis, Allergic Contact - immunology</subject><subject>Dermatitis, Allergic Contact - pathology</subject><subject>Dose-Response Relationship, Immunologic</subject><subject>Humans</subject><subject>Immunopathology</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Keratinocytes - immunology</subject><subject>Keratinocytes - pathology</subject><subject>Medical sciences</subject><subject>Oxidative Stress</subject><subject>Skin allergic diseases. Stinging insect allergies</subject><subject>T-Lymphocytes - immunology</subject><subject>Up-Regulation - immunology</subject><issn>0007-0963</issn><issn>1365-2133</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNqNkE1v1DAQhi0EKkvLT0DyAXFL8EccxwcOUGBLVRVVKuJovM64eJs4qe2FXX49SXe155488rzPzOhBCFNSUlLV79cl5bUoGOW8pEo1JWGEiXL7DC2OjedoQQiRBVE1f4lepbQmhHIiyAk6UYLXjLEF-nX7G_BoYvbWjyb7IeDB4TEOnXcQp48_gO8fizDYXYaEfcB5ZiL4vt8EwBHSOIQEOA84QUg--38-3GFzByGnM_TCmS7B68N7in58_XJ7flFcfV9-O_94VdiKU1FwAzWRTlSKyJY6KzlTajq_qaFauYa5hjSWAXWrWthWGtVSxmXrwFlllav4KXq3nzvd_rCBlHXvk4WuMwGGTdJSSdk0jE3BZh-0cUgpgtNj9L2JO02JnuXqtZ4d6tmhnuXqR7l6O6FvDjs2qx7aI3iwOfXfHvomWdO5aIL16RibB4pmjn3Yx_76DnZPXq8_XX6eq4kv9rxPGbZH3sR7XUsuhf55vdTk8oYrpi70kv8HsJmluw</recordid><startdate>199801</startdate><enddate>199801</enddate><creator>LITTLE, M. C</creator><creator>METCALFE, R. A</creator><creator>HAYCOCK, J. 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M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4315-3ae607f54907d1fc7329900086e4bf82f808c2e1fb65cd7a9d1237dfefc9c9f43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Allergens - immunology</topic><topic>Allergic diseases</topic><topic>Biological and medical sciences</topic><topic>Cell Adhesion - immunology</topic><topic>Cell Culture Techniques</topic><topic>Cell Differentiation - immunology</topic><topic>Cell Division - immunology</topic><topic>Cell Line</topic><topic>Cytokines - immunology</topic><topic>Dermatitis, Allergic Contact - immunology</topic><topic>Dermatitis, Allergic Contact - pathology</topic><topic>Dose-Response Relationship, Immunologic</topic><topic>Humans</topic><topic>Immunopathology</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Keratinocytes - immunology</topic><topic>Keratinocytes - pathology</topic><topic>Medical sciences</topic><topic>Oxidative Stress</topic><topic>Skin allergic diseases. Stinging insect allergies</topic><topic>T-Lymphocytes - immunology</topic><topic>Up-Regulation - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LITTLE, M. C</creatorcontrib><creatorcontrib>METCALFE, R. A</creatorcontrib><creatorcontrib>HAYCOCK, J. W</creatorcontrib><creatorcontrib>HEALY, J</creatorcontrib><creatorcontrib>GAWKRODGER, D. J</creatorcontrib><creatorcontrib>NEIL, S. M</creatorcontrib><collection>Istex</collection><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>MEDLINE - Academic</collection><jtitle>British journal of dermatology (1951)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LITTLE, M. 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M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The participation of proliferative keratinocytes in the preimmune response to sensitizing agents</atitle><jtitle>British journal of dermatology (1951)</jtitle><addtitle>British Journal of Dermatology</addtitle><date>1998-01</date><risdate>1998</risdate><volume>138</volume><issue>1</issue><spage>45</spage><epage>56</epage><pages>45-56</pages><issn>0007-0963</issn><eissn>1365-2133</eissn><coden>BJDEAZ</coden><notes>ark:/67375/WNG-0JQ3929H-G</notes><notes>ArticleID:BJD2025</notes><notes>istex:2FE96E5F87554EF5D7414D40D605AA0112819A48</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>The aims of this study were to investigate whether keratinocytes are capable of playing a direct preimmune role in the pathophysiology of allergic contact dermatitis (ACD) and to examine to what extent the degree of differentiation might influence this. We measured the ability of sensitizing agents to up‐regulate intercellular adhesion molecule 1 (ICAM‐1) expression in cultured normal human keratinocytes (NHK) and in the transformed human keratinocyte HaCaT cell line. In proliferative HaCaT cells, following a 24 h exposure, nickel compounds, para‐phenylenediamine (pPD) and 1‐chloro‐2,4‐dinitrobenzene produced a concentration‐dependent up‐regulation of ICAM‐1 expression without reducing cell viability, while K2Cr2O7 led to ICAM‐1 up‐regulation at cytotoxic concentrations, and CrCl3 was without effect. In NHK, NiSO4 and pPD induced ICAM‐1 expression to a significantly greater extent in proliferative cells than in differentiated cells, where involucrin expression was measured to assess the differentiation state. NiSO4‐ or pPD‐pretreatment of proliferative HaCaT cells enhanced T‐cell binding, which was abolished by neutralizing antibodies to ICAM‐1 or CD18. Our investigations concerning the involvement of oxidative stress in the induction of ICAM‐1 expression in response to sensitizing agents were inconclusive. The oxidizing agents FeCl3 and H2O2 up‐regulated ICAM‐1 expression in HaCaT cells but there was no clear relationship between the ability of agents to induce ICAM‐1 expression and their ability to alter the levels of reduced glutathione. Although pPD increased interleukin‐1α release from NHK, this cytokine was not capable of inducing ICAM‐1 expression in NHK. Tumour necrosis factor‐α, which does induce ICAM‐1 expression in NHK, was not detected in response to pPD, arguing against an autocrine pathway of ICAM‐1 induction in response to pPD. In summary, we report the direct interaction of sensitizing agents with keratinocytes leading to the generation of immune signals, particularly by proliferative keratinocytes, suggesting an active role for the proliferative keratinocyte in the pathophysiology of ACD.</abstract><cop>Oxford BSL</cop><pub>Blackwell Science Ltd</pub><pmid>9536222</pmid><doi>10.1046/j.1365-2133.1998.02025.x</doi><tpages>12</tpages></addata></record> |
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| ispartof | British journal of dermatology (1951), 1998-01, Vol.138 (1), p.45-56 |
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| language | eng |
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| source | Wiley-Blackwell Journals; Oxford Academic Journals (OUP) |
| subjects | Allergens - immunology Allergic diseases Biological and medical sciences Cell Adhesion - immunology Cell Culture Techniques Cell Differentiation - immunology Cell Division - immunology Cell Line Cytokines - immunology Dermatitis, Allergic Contact - immunology Dermatitis, Allergic Contact - pathology Dose-Response Relationship, Immunologic Humans Immunopathology Intercellular Adhesion Molecule-1 - metabolism Keratinocytes - immunology Keratinocytes - pathology Medical sciences Oxidative Stress Skin allergic diseases. Stinging insect allergies T-Lymphocytes - immunology Up-Regulation - immunology |
| title | The participation of proliferative keratinocytes in the preimmune response to sensitizing agents |
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