慢性烟雾暴露引起小鼠肺气肿伴淋巴滤泡形成

Chronic cigarette smoke exposure induces emphysema and lymphoid neogenesisin mice

目的研究不同时间慢性香烟烟雾暴露对小鼠肺气肿和淋巴滤泡形成的影响。方法6～8周龄SPF级近交系C57BL/6雌性小鼠24只,随机分组：12周暴露组、12周对照组、24周暴露组、24周对照组,观察12周和24周不同暴露时间小鼠肺气肿和肺淋巴滤泡新生情况,分析淋巴滤泡的细胞和分子构成。结果24周烟雾暴露小鼠的肺泡破坏指数（48.28±2.01）%高于12周烟雾暴露小鼠（33.85±0.84）%,肺气肿程度加重;12周的烟雾暴露不能使肺组织形成结构成熟的淋巴滤泡,但是经24周暴露后,小鼠肺组织形成典型的淋巴滤泡。淋巴滤泡主要由大量的B细胞、CD3^＋T细胞、CD4^＋T细胞、CD8^＋T细胞构成,少量基质细胞和CXCL13^＋细胞也参与了淋巴滤泡的形成。结论24周慢性烟雾暴露刺激可以导致小鼠肺组织结构破坏并伴淋巴滤泡形成。

Objective To study the effect of two different cigarette smoke exposure periods on the formation of lymphoid tissue. Methods Female C57BL/6 mice （ n = 24）, 6-8 week old, were randomly divided into 12 weeks smoke groups, 12 weeks control groups, 24 weeks smoke groups and 24 weeks control groups. To observe the changes of pulmonary emphysema and pulmonary lymph follicles in mice at 12 and 24 weeks. Results After smoke exposure, the smoke mice developed emphysema, which was more remarkable in 24 week exposure mice as compared to 12 week exposure mice; the corresponding damage index was （48.28±2.01） % and （33.85±0.84） % respectively. Mature lymphoid follicles were present in 24 week exposure mice only, but not in 12 week exposure mice. Lymphoid follicles were formed by a large number of B and T cells, with stromal cells and CXCL13^＋ cells to a lesser degree. Conclusions 24 weeks of mice receiving chronic cigarette smoke developed well-formed lymphoid tissues in the lung tissue together with emphysema.