慢性阻塞性肺病
免疫组织化学
嗜酸性粒细胞
医学
气道
基底膜
内科学
病理
免疫学
哮喘
外科
作者
Sophie Booth,Danen Cunoosamy,Jørgen Vestbo,Dave Singh,Andrew Higham
标识
DOI:10.1183/13993003.congress-2023.oa4298
摘要
Background: Small airway (SA) epithelial IL-33 expression has previously been shown to be increased in very severe COPD. Little is known about the relationship between smoking or eosinophils on SA IL-33 expression in COPD. Aims: To quantify SA IL-33 expression in COPD vs controls and investigate the effect of current smoking and eosinophil counts on IL-33 expression. We explored the relationship between IL-33 and epithelial thickness. Methods: IL-33 expression was identified in the SA of smoking controls (n=23) and COPD patients (GOLD I-III) (n=24) by immunohistochemistry and presented as the average number of cells per mm basement membrane. Results: There were no significant differences in epithelial IL-33 expression between COPD or controls. No relationship between smoking or eosinophils and IL-33 expression was observed (p>0.05). However, there was a significant correlation between IL-33 and epithelial thickness in both COPD and controls (rho=0.61-0.72, p<0.01) (Figure 1) and we observed overexpression of IL-33 in areas of epithelial remodelling. Figure 1: A) Smoking Controls, B) COPD Conclusion: SA IL-33 expression is related to epithelial remodelling in COPD.
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