Comparative Study of Ectopic Lymphoid Aggregates in Sheep and Murine Models of Bleomycin-Induced Pulmonary Fibrosis.

IF 2.1 4区 医学 Q3 RESPIRATORY SYSTEM
Udari Eshani Perera, Louise Organ, Simon G Royce, Chrishan S Samuel, Habtamu B Derseh, Sasika N V Dewage, Emmanuel Koumoundouros, Andrew Stent, Kenneth J Snibson
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Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic disease characterized by excessive deposition of extracellular matrix in the interstitial lung parenchyma, often manifested by dyspnea and progressive loss of lung function. The role of inflammation in the pathogenesis of IPF is not well understood. This study evaluated the histopathological and inflammatory components of bleomycin-induced pulmonary fibrosis in mouse and sheep models, in terms of their ability to translate to the human IPF. Merino sheep (n = 8) were bronchoscopically administered with two bleomycin infusions, two weeks apart, into a caudal lung segment, with a saline (control) administered into a caudal segment in the opposite lung. Balb/c mice were twice intranasally instilled, one week apart, with either bleomycin (n = 7); or saline (control, n = 7). Lung samples were taken for the histopathological assessment 28 days in sheep and 21 days in mice after the first bleomycin administration. We observed tertiary lymphoid aggregates, in the fibrotic lung parenchyma of sheep, but not in mouse lung tissues exposed to bleomycin. B-cell and T-cell infiltration significantly increased in sheep lung tissues compared to mouse lung tissues due to bleomycin injury. Statistical analysis showed that the fibrotic score, fibrotic fraction, and tissue fraction significantly increased in sheep lung tissues compared to murine lung tissues. The presence of tertiary lymphoid aggregates in the lung parenchyma and increased infiltration of T-cells and B-cells, in the sheep model, may be useful for the future study of the underlying inflammatory disease mechanisms in the lung parenchyma of IPF patients.

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博莱霉素诱导的绵羊和小鼠肺纤维化模型异位淋巴聚集体的比较研究。
特发性肺纤维化(Idiopathic pulmonary fibrosis, IPF)是一种以肺间质间质细胞外基质过度沉积为特征的慢性疾病,常表现为呼吸困难和肺功能进行性丧失。炎症在IPF发病机制中的作用尚不清楚。本研究评估了博莱霉素在小鼠和绵羊模型中诱导肺纤维化的组织病理学和炎症成分,以及它们转化为人类IPF的能力。在支气管镜下,将8只美利奴羊(n = 8)两次博来霉素输注至尾侧肺段,间隔两周,并将生理盐水(对照组)输注至对侧肺尾侧肺段。Balb/c小鼠两次鼻内灌注博莱霉素,间隔一周;或生理盐水(对照组,n = 7)。第一次给予博来霉素后28天和小鼠21天分别取肺标本进行组织病理学评估。我们在绵羊的纤维化肺实质中观察到三级淋巴样聚集体,但在暴露于博来霉素的小鼠肺组织中没有观察到。博来霉素损伤后,绵羊肺组织中b细胞和t细胞的浸润量明显高于小鼠肺组织。统计分析表明,与小鼠肺组织相比,绵羊肺组织的纤维化评分、纤维化分数和组织分数均显著升高。在绵羊模型中,肺实质中存在三级淋巴样聚集体,t细胞和b细胞浸润增加,可能有助于未来研究IPF患者肺实质中潜在的炎症疾病机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Canadian respiratory journal
Canadian respiratory journal 医学-呼吸系统
CiteScore
4.20
自引率
0.00%
发文量
61
审稿时长
6-12 weeks
期刊介绍: Canadian Respiratory Journal is a peer-reviewed, Open Access journal that aims to provide a multidisciplinary forum for research in all areas of respiratory medicine. The journal publishes original research articles, review articles, and clinical studies related to asthma, allergy, COPD, non-invasive ventilation, therapeutic intervention, lung cancer, airway and lung infections, as well as any other respiratory diseases.
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