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| Open AccessThe establishment of COPD organoids to study host-pathogen interaction reveals enhanced viral fitness of SARS-CoV-2 in bronchi
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory respiratory disease characterized by airflow limitation and infective exacerbations. Here, Chan et al. report the generation of nasopharyngeal and bronchial COPD organoids derived from adult stem cells and employ them in the study of host-pathogen interactions, including SARS-CoV-2 and Pseudomonas aeruginosa.
- Louisa L. Y. Chan
- , Danielle E. Anderson
- & Sanjay H. Chotirmall
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| Open AccessThe arginine methyltransferase PRMT7 promotes extravasation of monocytes resulting in tissue injury in COPD
Chronic obstructive pulmonary disease is a progressive and incurable chronic condition that involves accumulation of inflammatory macrophages in the lung tissue. Authors here show in mouse models of lung disease that PRMT7, a protein arginine methyltransferase, is an important regulator of recruitment and the pro-inflammatory phenotype of macrophages.
- Gizem Günes Günsel
- , Thomas M. Conlon
- & Ali Önder Yildirim
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| Open AccessCharacterization of the COPD alveolar niche using single-cell RNA sequencing
Chronic obstructive pulmonary disease is a leading cause of death worldwide, while our understanding of cell-specific mechanisms underlying its pathobiology remains incomplete. Here the authors perform scRNA-seq of human lung tissue to identify transcriptional changes in alveolar niche cells associated with the disease.
- Maor Sauler
- , John E. McDonough
- & Ivan O. Rosas
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| Open AccessEpigenetic reprogramming of airway macrophages promotes polarization and inflammation in muco-obstructive lung disease
Muco-obstructive lung diseases are characterised by airway macrophage (AM) populations which may have epigenetic changes. Here using a mouse model the authors show epigenetic alteration of AMs with changes in LPS response, phagocytosis and efferocytosis similar to culture with mucus in vitro.
- Joschka Hey
- , Michelle Paulsen
- & Marcus A. Mall
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| Open AccessAn innate contribution of human nicotinic receptor polymorphisms to COPD-like lesions
Human polymorphisms in nicotinic acetylcholine receptor genes have been linked to both smoking and lung diseases like Chronic Obstructive Pulmonary Disease (COPD) or lung cancer. Here the authors identify a direct role for a human coding polymorphism in COPD-like lesions independent of smoke or nicotine exposure.
- Julie Routhier
- , Stéphanie Pons
- & Uwe Maskos
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| Open AccessWhole genome sequence analysis of pulmonary function and COPD in 19,996 multi-ethnic participants
Chronic obstructive pulmonary disease is a leading cause of morbidity and mortality. Here, the authors analyse whole genome sequence data and find new loci associated with lung function and COPD.
- Xutong Zhao
- , Dandi Qiao
- & Ani Manichaikul
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| Open AccessDiscovering the genes mediating the interactions between chronic respiratory diseases in the human interactome
Complex diseases often share genetic determinants and symptoms, but the mechanistic basis of disease interactions remains elusive. Here, the authors propose a network topological measure to identify proteins linking complex diseases in the interactome, and identify mediators between COPD and asthma.
- Enrico Maiorino
- , Seung Han Baek
- & Amitabh Sharma
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| Open AccessInvolvement of cigarette smoke-induced epithelial cell ferroptosis in COPD pathogenesis
Altered iron homeostasis resulting in excessive oxidative stress has been implicated in smoke-induced lung diseases. Here the authors show that ferroptosis of lung epithelial cells, potentially resulting from excessive ferritinophagy, is involved in the pathogenesis of COPD.
- Masahiro Yoshida
- , Shunsuke Minagawa
- & Kazuyoshi Kuwano
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Article
| Open AccessSTING-dependent sensing of self-DNA drives silica-induced lung inflammation
Silica particles induce intereukin-1 (IL-1) response to contribute to lung inflammation, but the underlying mechanism is unclear. Here the authors show that silica induces cell death and release of mitochondria and genomic DNA, which are sensed by STING with or without involving cGAS, respectively, for IL-1 induction and lung inflammation.
- Sulayman Benmerzoug
- , Stéphanie Rose
- & Valerie F. J. Quesniaux