Inflammation in acne scarring: a comparison of the responses in lesions from patients prone and not prone to scar
Summary Background Many patients with inflammatory acne suffer from significant scarring, which is disfiguring and difficult to treat. A cell‐mediated immune response is considered to be involved in the pathogenesis of acne, although the extent of this response has been found to differ among patien...
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| Veröffentlicht in: | British journal of dermatology (1951) 2004-01, Vol.150 (1), p.72-81 |
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| container_title | British journal of dermatology (1951) |
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| creator | Holland, D.B. Jeremy, A.H.T. Roberts, S.G. Seukeran, D.C. Layton, A.M. Cunliffe, W.J. |
| description | Summary
Background Many patients with inflammatory acne suffer from significant scarring, which is disfiguring and difficult to treat. A cell‐mediated immune response is considered to be involved in the pathogenesis of acne, although the extent of this response has been found to differ among patients.
Objective To assess whether there were differences in the cell‐mediated immune responses at different time points in inflamed lesion development and resolution in patients who were prone (S patients) and those with the same degree of inflamed acne who were not prone (NS patients) to develop scarring.
Methods Cellular and vascular markers were investigated using standard immunohistochemical techniques on biopsies of inflamed lesions of known duration, i.e. |
| doi_str_mv | 10.1111/j.1365-2133.2004.05749.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_80120792</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>552711231</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4899-51b56f222ed35280f525a02ba4b8b23f998764744080c7990a81821d1f8110533</originalsourceid><addsrcrecordid>eNqNkc1u1DAUhS0EokPhFZCFBLuE67_ERmIBA5SWoWxAXVpOxoYMiZ3aGTF9e5xO1Eqs8Ma27neOr89FCBMoSV6vdyVhlSgoYaykALwEUXNVHh6g1V3hIVoBQF2AqtgJepLSDoAwEPAYnRBe86oiaoWuz73rzTCYqQsedx6b1lucWhNj53--wQa3YRhN7FIuB4enXxZHm8bgk00z39uUlQm7GAY8Zhvrp4THGLKN8Vvsw7TcpnDr-xQ9cqZP9tmyn6Ifnz5-X38uNt_OztfvNkXLpVKFII2oHKXUbpmgEpygwgBtDG9kQ5lTStZV_gYHCW2tFBhJJCVb4iQhIBg7Ra-Ovvn1671Nkx661Nq-N96GfdISCIVa0Qy--AfchX30uTedswUhFOMZkkeojSGlaJ0eYzeYeKMJ6Hkmeqfn6PUc_azj-nYm-pClzxf_fTPY7b1wGUIGXi6AyQH1LhrfdumeE4JwVVeZe3vk_nS9vfnvBvT7iw_zKeuLo75Lkz3c6U38raua1UJfXZ7pLxfrK3a5qfRX9hdML7Tf</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>200055934</pqid></control><display><type>article</type><title>Inflammation in acne scarring: a comparison of the responses in lesions from patients prone and not prone to scar</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Holland, D.B. ; Jeremy, A.H.T. ; Roberts, S.G. ; Seukeran, D.C. ; Layton, A.M. ; Cunliffe, W.J.</creator><creatorcontrib>Holland, D.B. ; Jeremy, A.H.T. ; Roberts, S.G. ; Seukeran, D.C. ; Layton, A.M. ; Cunliffe, W.J.</creatorcontrib><description>Summary
Background Many patients with inflammatory acne suffer from significant scarring, which is disfiguring and difficult to treat. A cell‐mediated immune response is considered to be involved in the pathogenesis of acne, although the extent of this response has been found to differ among patients.
Objective To assess whether there were differences in the cell‐mediated immune responses at different time points in inflamed lesion development and resolution in patients who were prone (S patients) and those with the same degree of inflamed acne who were not prone (NS patients) to develop scarring.
Methods Cellular and vascular markers were investigated using standard immunohistochemical techniques on biopsies of inflamed lesions of known duration, i.e. < 6 h (n = 14), 24 h (n = 14), 48 h (n = 10), 72 h (n = 10) and 6–7 days (n = 11) from the backs of acne patients.
Results In early lesions from NS patients there was a large influx of CD4+ T cells, macrophages and Langerhans cells with a high number of cells expressing HLA‐DR. Also there was significant angiogenesis and vascular adhesion molecule expression. Cell recruitment peaked in 48 h lesions, after which leucocyte numbers decreased and vascular activity returned to normal. Of the T cells, only 50% were memory/effector (CD45RO+) and naive (CD45RA+) cells, while the remainder were unclassified (CD45RO–, CD45RA–). In early lesions from S patients, CD4+ T cell numbers were smaller, although a high proportion were skin homing memory/effector cells. Langerhans cell numbers and cellular HLA‐DR expression were low, while numbers of macrophages, blood vessels and vascular adhesion molecules were high. In resolving lesions angiogenesis remained high, with a further influx of macrophages and skin homing memory/effector cells and increased cellular HLA‐DR expression.
Conclusions The cellular infiltrate was large and active with a greater nonspecific response (few memory T cells) in early lesions of NS patients, which subsided in resolution. In contrast, a predominantly specific immune response was present in S patients, which was initially smaller and ineffective, but was increased and activated in resolving lesions. Such excessive inflammation in healing tissue is conducive to scarring and suggests that the use of topical anti‐inflammatory treatments would be appropriate for these patients.</description><identifier>ISSN: 0007-0963</identifier><identifier>EISSN: 1365-2133</identifier><identifier>DOI: 10.1111/j.1365-2133.2004.05749.x</identifier><identifier>PMID: 14746619</identifier><identifier>CODEN: BJDEAZ</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>acne ; Acne Vulgaris - complications ; Acne Vulgaris - immunology ; Adolescent ; Adult ; Biological and medical sciences ; Cell Adhesion Molecules - metabolism ; Cicatrix - etiology ; Cicatrix - genetics ; Cicatrix - immunology ; Dermatology ; Female ; Genetic Predisposition to Disease ; HLA-DR Antigens - analysis ; Humans ; Immunity, Cellular ; Immunoenzyme Techniques ; Inflammation - etiology ; Inflammation - immunology ; Langerhans Cells - immunology ; macrophages ; Macrophages - immunology ; Male ; Medical sciences ; scarring ; skin homing memory/effector T cells ; Skin involvement in other diseases. Miscellaneous. General aspects ; T-Lymphocyte Subsets - immunology</subject><ispartof>British journal of dermatology (1951), 2004-01, Vol.150 (1), p.72-81</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright Blackwell Scientific Publications Ltd. Jan 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4899-51b56f222ed35280f525a02ba4b8b23f998764744080c7990a81821d1f8110533</citedby><cites>FETCH-LOGICAL-c4899-51b56f222ed35280f525a02ba4b8b23f998764744080c7990a81821d1f8110533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2133.2004.05749.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2133.2004.05749.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,4010,27900,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15514976$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14746619$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Holland, D.B.</creatorcontrib><creatorcontrib>Jeremy, A.H.T.</creatorcontrib><creatorcontrib>Roberts, S.G.</creatorcontrib><creatorcontrib>Seukeran, D.C.</creatorcontrib><creatorcontrib>Layton, A.M.</creatorcontrib><creatorcontrib>Cunliffe, W.J.</creatorcontrib><title>Inflammation in acne scarring: a comparison of the responses in lesions from patients prone and not prone to scar</title><title>British journal of dermatology (1951)</title><addtitle>Br J Dermatol</addtitle><description>Summary
Background Many patients with inflammatory acne suffer from significant scarring, which is disfiguring and difficult to treat. A cell‐mediated immune response is considered to be involved in the pathogenesis of acne, although the extent of this response has been found to differ among patients.
Objective To assess whether there were differences in the cell‐mediated immune responses at different time points in inflamed lesion development and resolution in patients who were prone (S patients) and those with the same degree of inflamed acne who were not prone (NS patients) to develop scarring.
Methods Cellular and vascular markers were investigated using standard immunohistochemical techniques on biopsies of inflamed lesions of known duration, i.e. < 6 h (n = 14), 24 h (n = 14), 48 h (n = 10), 72 h (n = 10) and 6–7 days (n = 11) from the backs of acne patients.
Results In early lesions from NS patients there was a large influx of CD4+ T cells, macrophages and Langerhans cells with a high number of cells expressing HLA‐DR. Also there was significant angiogenesis and vascular adhesion molecule expression. Cell recruitment peaked in 48 h lesions, after which leucocyte numbers decreased and vascular activity returned to normal. Of the T cells, only 50% were memory/effector (CD45RO+) and naive (CD45RA+) cells, while the remainder were unclassified (CD45RO–, CD45RA–). In early lesions from S patients, CD4+ T cell numbers were smaller, although a high proportion were skin homing memory/effector cells. Langerhans cell numbers and cellular HLA‐DR expression were low, while numbers of macrophages, blood vessels and vascular adhesion molecules were high. In resolving lesions angiogenesis remained high, with a further influx of macrophages and skin homing memory/effector cells and increased cellular HLA‐DR expression.
Conclusions The cellular infiltrate was large and active with a greater nonspecific response (few memory T cells) in early lesions of NS patients, which subsided in resolution. In contrast, a predominantly specific immune response was present in S patients, which was initially smaller and ineffective, but was increased and activated in resolving lesions. Such excessive inflammation in healing tissue is conducive to scarring and suggests that the use of topical anti‐inflammatory treatments would be appropriate for these patients.</description><subject>acne</subject><subject>Acne Vulgaris - complications</subject><subject>Acne Vulgaris - immunology</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Cicatrix - etiology</subject><subject>Cicatrix - genetics</subject><subject>Cicatrix - immunology</subject><subject>Dermatology</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>HLA-DR Antigens - analysis</subject><subject>Humans</subject><subject>Immunity, Cellular</subject><subject>Immunoenzyme Techniques</subject><subject>Inflammation - etiology</subject><subject>Inflammation - immunology</subject><subject>Langerhans Cells - immunology</subject><subject>macrophages</subject><subject>Macrophages - immunology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>scarring</subject><subject>skin homing memory/effector T cells</subject><subject>Skin involvement in other diseases. Miscellaneous. General aspects</subject><subject>T-Lymphocyte Subsets - immunology</subject><issn>0007-0963</issn><issn>1365-2133</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS0EokPhFZCFBLuE67_ERmIBA5SWoWxAXVpOxoYMiZ3aGTF9e5xO1Eqs8Ma27neOr89FCBMoSV6vdyVhlSgoYaykALwEUXNVHh6g1V3hIVoBQF2AqtgJepLSDoAwEPAYnRBe86oiaoWuz73rzTCYqQsedx6b1lucWhNj53--wQa3YRhN7FIuB4enXxZHm8bgk00z39uUlQm7GAY8Zhvrp4THGLKN8Vvsw7TcpnDr-xQ9cqZP9tmyn6Ifnz5-X38uNt_OztfvNkXLpVKFII2oHKXUbpmgEpygwgBtDG9kQ5lTStZV_gYHCW2tFBhJJCVb4iQhIBg7Ra-Ovvn1671Nkx661Nq-N96GfdISCIVa0Qy--AfchX30uTedswUhFOMZkkeojSGlaJ0eYzeYeKMJ6Hkmeqfn6PUc_azj-nYm-pClzxf_fTPY7b1wGUIGXi6AyQH1LhrfdumeE4JwVVeZe3vk_nS9vfnvBvT7iw_zKeuLo75Lkz3c6U38raua1UJfXZ7pLxfrK3a5qfRX9hdML7Tf</recordid><startdate>200401</startdate><enddate>200401</enddate><creator>Holland, D.B.</creator><creator>Jeremy, A.H.T.</creator><creator>Roberts, S.G.</creator><creator>Seukeran, D.C.</creator><creator>Layton, A.M.</creator><creator>Cunliffe, W.J.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Oxford University Press</general><scope>BSCLL</scope><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>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>200401</creationdate><title>Inflammation in acne scarring: a comparison of the responses in lesions from patients prone and not prone to scar</title><author>Holland, D.B. ; Jeremy, A.H.T. ; Roberts, S.G. ; Seukeran, D.C. ; Layton, A.M. ; Cunliffe, W.J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4899-51b56f222ed35280f525a02ba4b8b23f998764744080c7990a81821d1f8110533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>acne</topic><topic>Acne Vulgaris - complications</topic><topic>Acne Vulgaris - immunology</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Cicatrix - etiology</topic><topic>Cicatrix - genetics</topic><topic>Cicatrix - immunology</topic><topic>Dermatology</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>HLA-DR Antigens - analysis</topic><topic>Humans</topic><topic>Immunity, Cellular</topic><topic>Immunoenzyme Techniques</topic><topic>Inflammation - etiology</topic><topic>Inflammation - immunology</topic><topic>Langerhans Cells - immunology</topic><topic>macrophages</topic><topic>Macrophages - immunology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>scarring</topic><topic>skin homing memory/effector T cells</topic><topic>Skin involvement in other diseases. Miscellaneous. General aspects</topic><topic>T-Lymphocyte Subsets - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Holland, D.B.</creatorcontrib><creatorcontrib>Jeremy, A.H.T.</creatorcontrib><creatorcontrib>Roberts, S.G.</creatorcontrib><creatorcontrib>Seukeran, D.C.</creatorcontrib><creatorcontrib>Layton, A.M.</creatorcontrib><creatorcontrib>Cunliffe, W.J.</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</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>Holland, D.B.</au><au>Jeremy, A.H.T.</au><au>Roberts, S.G.</au><au>Seukeran, D.C.</au><au>Layton, A.M.</au><au>Cunliffe, W.J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inflammation in acne scarring: a comparison of the responses in lesions from patients prone and not prone to scar</atitle><jtitle>British journal of dermatology (1951)</jtitle><addtitle>Br J Dermatol</addtitle><date>2004-01</date><risdate>2004</risdate><volume>150</volume><issue>1</issue><spage>72</spage><epage>81</epage><pages>72-81</pages><issn>0007-0963</issn><eissn>1365-2133</eissn><coden>BJDEAZ</coden><abstract>Summary
Background Many patients with inflammatory acne suffer from significant scarring, which is disfiguring and difficult to treat. A cell‐mediated immune response is considered to be involved in the pathogenesis of acne, although the extent of this response has been found to differ among patients.
Objective To assess whether there were differences in the cell‐mediated immune responses at different time points in inflamed lesion development and resolution in patients who were prone (S patients) and those with the same degree of inflamed acne who were not prone (NS patients) to develop scarring.
Methods Cellular and vascular markers were investigated using standard immunohistochemical techniques on biopsies of inflamed lesions of known duration, i.e. < 6 h (n = 14), 24 h (n = 14), 48 h (n = 10), 72 h (n = 10) and 6–7 days (n = 11) from the backs of acne patients.
Results In early lesions from NS patients there was a large influx of CD4+ T cells, macrophages and Langerhans cells with a high number of cells expressing HLA‐DR. Also there was significant angiogenesis and vascular adhesion molecule expression. Cell recruitment peaked in 48 h lesions, after which leucocyte numbers decreased and vascular activity returned to normal. Of the T cells, only 50% were memory/effector (CD45RO+) and naive (CD45RA+) cells, while the remainder were unclassified (CD45RO–, CD45RA–). In early lesions from S patients, CD4+ T cell numbers were smaller, although a high proportion were skin homing memory/effector cells. Langerhans cell numbers and cellular HLA‐DR expression were low, while numbers of macrophages, blood vessels and vascular adhesion molecules were high. In resolving lesions angiogenesis remained high, with a further influx of macrophages and skin homing memory/effector cells and increased cellular HLA‐DR expression.
Conclusions The cellular infiltrate was large and active with a greater nonspecific response (few memory T cells) in early lesions of NS patients, which subsided in resolution. In contrast, a predominantly specific immune response was present in S patients, which was initially smaller and ineffective, but was increased and activated in resolving lesions. Such excessive inflammation in healing tissue is conducive to scarring and suggests that the use of topical anti‐inflammatory treatments would be appropriate for these patients.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>14746619</pmid><doi>10.1111/j.1365-2133.2004.05749.x</doi><tpages>10</tpages></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | acne Acne Vulgaris - complications Acne Vulgaris - immunology Adolescent Adult Biological and medical sciences Cell Adhesion Molecules - metabolism Cicatrix - etiology Cicatrix - genetics Cicatrix - immunology Dermatology Female Genetic Predisposition to Disease HLA-DR Antigens - analysis Humans Immunity, Cellular Immunoenzyme Techniques Inflammation - etiology Inflammation - immunology Langerhans Cells - immunology macrophages Macrophages - immunology Male Medical sciences scarring skin homing memory/effector T cells Skin involvement in other diseases. Miscellaneous. General aspects T-Lymphocyte Subsets - immunology |
| title | Inflammation in acne scarring: a comparison of the responses in lesions from patients prone and not prone to scar |
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