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Ferret models of alpha-1 antitrypsin deficiency develop lung and liver disease
Journal article   Open access   Peer reviewed

Ferret models of alpha-1 antitrypsin deficiency develop lung and liver disease

Nan He, Xiaoming Liu, Amber R Vegter, T Idil A Evans, Jaimie S Gray, Junfeng Guo, Shashanna R Moll, Lydia J Guo, Meihui Luo, Ningxia Ma, …
JCI insight, Vol.7(5), e143004
03/08/2022
DOI: 10.1172/jci.insight.143004
PMCID: PMC8983124
PMID: 35104244
url
https://doi.org/10.1172/jci.insight.143004View
Published (Version of record) Open Access

Abstract

Alpha-1 antitrypsin deficiency (AATD) is the most common genetic cause and risk factor for chronic obstructive pulmonary disease, but the field lacks a large-animal model that allows for longitudinal assessment of pulmonary function. We hypothesized that ferrets would model human AATD-related lung and hepatic disease. AAT-knockout (AAT-KO) and PiZZ (E342K, the most common mutation in humans) ferrets were generated and compared with matched controls using custom-designed flexiVent modules to perform pulmonary function tests, quantitative computed tomography (QCT), bronchoalveolar lavage (BAL) proteomics, and alveolar morphometry. Complete loss of AAT (AAT-KO) led to increased pulmonary compliance and expiratory airflow limitation, consistent with obstructive lung disease. QCT and morphometry confirmed emphysema and airspace enlargement, respectively. Pathway analysis of BAL proteomics data revealed inflammatory lung disease and impaired cellular migration. The PiZ mutation resulted in altered AAT protein folding in the liver, hepatic injury, and reduced plasma concentrations of AAT, and PiZZ ferrets developed obstructive lung disease. In summary, AAT-KO and PiZZ ferrets model the progressive obstructive pulmonary disease seen in AAT-deficient patients and may serve as a platform for preclinical testing of therapeutics including gene therapy.
Pulmonology Genetic diseases Proteases COPD

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