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ß1 Integrin regulates adult lung alveolar epithelial cell inflammation.
Authors Plosa EJ, Benjamin JT, Sucre JM, Gulleman PM, Gleaves LA, Han W, Kook S,
Polosukhin VV, Haake SM, Guttentag SH, Young LR, Pozzi A, Blackwell TS, Zent R
Submitted By Submitted Externally on 4/6/2020
Status Published
Journal JCI insight
Year 2020
Date Published 1/1/2020
Volume : Pages 5 : Not Specified
PubMed Reference 31873073
Abstract Integrins, the extracellular matrix receptors that facilitate cell adhesion and
migration, are necessary for organ morphogenesis; however, their role in
maintaining adult tissue homeostasis is poorly understood. To define the
functional importance of ß1 integrin in adult mouse lung, we deleted it after
completion of development in type 2 alveolar epithelial cells (AECs). Aged ß1
integrin-deficient mice exhibited chronic obstructive pulmonary disease-like
(COPD-like) pathology characterized by emphysema, lymphoid aggregates, and
increased macrophage infiltration. These histopathological abnormalities were
preceded by ß1 integrin-deficient AEC dysfunction such as excessive ROS
production and upregulation of NF-?B-dependent chemokines, including CCL2.
Genetic deletion of the CCL2 receptor, Ccr2, in mice with ß1 integrin-deficient
type 2 AECs impaired recruitment of monocyte-derived macrophages and resulted in
accelerated inflammation and severe premature emphysematous destruction. The
lungs exhibited reduced AEC efferocytosis and excessive numbers of inflamed type
2 AECs, demonstrating the requirement for recruited monocytes/macrophages in
limiting lung injury and remodeling in the setting of a chronically inflamed
epithelium. These studies support a critical role for ß1 integrin in alveolar
homeostasis in the adult lung.


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