Ola Ahmed Bakry, Rehab Monir Samaka, Hend Sebika, Iman Seleit
{"title":"toll样受体2和痤疮:它们是否会引发初始寻常性痤疮病变?","authors":"Ola Ahmed Bakry, Rehab Monir Samaka, Hend Sebika, Iman Seleit","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To elucidate the role of toll-like receptor 2 (TLR2) in the pathogenesis of acne vulgaris through its immunohistochemical localization in inflammatory and noninflammatory lesions of this disease entity.</p><p><strong>Study design: </strong>Using standard immunohistochemical techniques, we examined 30 acne cases (involved and noninvolved skin) and the normal skin biopsies of 30 sex- and age-matched, healthy subjects representing the control group.</p><p><strong>Results: </strong>All examined cases showed positive TLR2 expression in epidermis, pilosebaceous units and dermal inflammatory infiltrate. There were statistically significant differences between acne-involved skin and normal skin and between acne-involved and noninvolved skin regarding TLR2 expression intensity in pilosebaceous units (p < 0.001 for both) and dermal inflammatory infiltrate (p < 0.001 for both). Intense TLR2 expression was in favor of inflammatory acne lesions in pilosebaceous units (p = 0.03) and dermal inflammatory infiltrate (p < 0.05). Intense TLR2 expression was also in favor of severe acne lesions in pilosebaceous units (p = 0.0002) and dermal inflammatory infiltrate (p = 0.001).</p><p><strong>Conclusion: </strong>TLR2 is involved in the pathogenesis of inflammatory and noninflammatory acne lesions. This occurs through Propionibacterium acnes-mediated activation with the resultant release of inflammatory cytokines.</p>","PeriodicalId":55517,"journal":{"name":"Analytical and Quantitative Cytopathology and Histopathology","volume":"36 2","pages":"100-10"},"PeriodicalIF":0.1000,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Toll-like receptor 2 and P. acnes: do they trigger initial acne vulgaris lesions?\",\"authors\":\"Ola Ahmed Bakry, Rehab Monir Samaka, Hend Sebika, Iman Seleit\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To elucidate the role of toll-like receptor 2 (TLR2) in the pathogenesis of acne vulgaris through its immunohistochemical localization in inflammatory and noninflammatory lesions of this disease entity.</p><p><strong>Study design: </strong>Using standard immunohistochemical techniques, we examined 30 acne cases (involved and noninvolved skin) and the normal skin biopsies of 30 sex- and age-matched, healthy subjects representing the control group.</p><p><strong>Results: </strong>All examined cases showed positive TLR2 expression in epidermis, pilosebaceous units and dermal inflammatory infiltrate. There were statistically significant differences between acne-involved skin and normal skin and between acne-involved and noninvolved skin regarding TLR2 expression intensity in pilosebaceous units (p < 0.001 for both) and dermal inflammatory infiltrate (p < 0.001 for both). Intense TLR2 expression was in favor of inflammatory acne lesions in pilosebaceous units (p = 0.03) and dermal inflammatory infiltrate (p < 0.05). Intense TLR2 expression was also in favor of severe acne lesions in pilosebaceous units (p = 0.0002) and dermal inflammatory infiltrate (p = 0.001).</p><p><strong>Conclusion: </strong>TLR2 is involved in the pathogenesis of inflammatory and noninflammatory acne lesions. This occurs through Propionibacterium acnes-mediated activation with the resultant release of inflammatory cytokines.</p>\",\"PeriodicalId\":55517,\"journal\":{\"name\":\"Analytical and Quantitative Cytopathology and Histopathology\",\"volume\":\"36 2\",\"pages\":\"100-10\"},\"PeriodicalIF\":0.1000,\"publicationDate\":\"2014-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Analytical and Quantitative Cytopathology and Histopathology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Analytical and Quantitative Cytopathology and Histopathology","FirstCategoryId":"3","ListUrlMain":"","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
Toll-like receptor 2 and P. acnes: do they trigger initial acne vulgaris lesions?
Objective: To elucidate the role of toll-like receptor 2 (TLR2) in the pathogenesis of acne vulgaris through its immunohistochemical localization in inflammatory and noninflammatory lesions of this disease entity.
Study design: Using standard immunohistochemical techniques, we examined 30 acne cases (involved and noninvolved skin) and the normal skin biopsies of 30 sex- and age-matched, healthy subjects representing the control group.
Results: All examined cases showed positive TLR2 expression in epidermis, pilosebaceous units and dermal inflammatory infiltrate. There were statistically significant differences between acne-involved skin and normal skin and between acne-involved and noninvolved skin regarding TLR2 expression intensity in pilosebaceous units (p < 0.001 for both) and dermal inflammatory infiltrate (p < 0.001 for both). Intense TLR2 expression was in favor of inflammatory acne lesions in pilosebaceous units (p = 0.03) and dermal inflammatory infiltrate (p < 0.05). Intense TLR2 expression was also in favor of severe acne lesions in pilosebaceous units (p = 0.0002) and dermal inflammatory infiltrate (p = 0.001).
Conclusion: TLR2 is involved in the pathogenesis of inflammatory and noninflammatory acne lesions. This occurs through Propionibacterium acnes-mediated activation with the resultant release of inflammatory cytokines.