{"title":"A role for neutrophil elastase in solar elastosis.","authors":"B. Starcher, M. Conrad","doi":"10.1002/9780470514771.CH18","DOIUrl":null,"url":null,"abstract":"Hairless (SKH-1) mice were mated with beige (C57BL/bb) mice to produce a hairless mouse deficient in neutrophil elastase (hhbb). These mice were exposed to 0.09 J UVB radiation for 5 months to see if neutrophil elastase was an important factor in the development of solar elastosis. Analysis of peritoneal neutrophils confirmed that the hhbb mouse was deficient in elastase, retaining only 10% of the activity of the normal littermates (hhHb). Skin myeloperoxidase activity was equally elevated in all the mice receiving UVB indicating a similar influx of inflammatory cells. The absolute breaking strength of the skin in both the hhBb and hhbb mice was not altered by UVB treatment over the 5 month exposure period. Elastin quantitated biochemically as desmosine, or visualized histologically, was increased following UVB exposure in the normal mice. In the elastase-deficient mice, however, the elastin fibres appeared to be unaffected by exposure to UVB radiation at this level. The results suggest that neutrophil elastase is an important mediator in the development of solar elastosis resulting from continued exposure to UVB.","PeriodicalId":10218,"journal":{"name":"Ciba Foundation symposium","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2007-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"35","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Ciba Foundation symposium","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/9780470514771.CH18","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 35
Abstract
Hairless (SKH-1) mice were mated with beige (C57BL/bb) mice to produce a hairless mouse deficient in neutrophil elastase (hhbb). These mice were exposed to 0.09 J UVB radiation for 5 months to see if neutrophil elastase was an important factor in the development of solar elastosis. Analysis of peritoneal neutrophils confirmed that the hhbb mouse was deficient in elastase, retaining only 10% of the activity of the normal littermates (hhHb). Skin myeloperoxidase activity was equally elevated in all the mice receiving UVB indicating a similar influx of inflammatory cells. The absolute breaking strength of the skin in both the hhBb and hhbb mice was not altered by UVB treatment over the 5 month exposure period. Elastin quantitated biochemically as desmosine, or visualized histologically, was increased following UVB exposure in the normal mice. In the elastase-deficient mice, however, the elastin fibres appeared to be unaffected by exposure to UVB radiation at this level. The results suggest that neutrophil elastase is an important mediator in the development of solar elastosis resulting from continued exposure to UVB.