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AMD3100 ameliorates cigarette smoke-induced emphysema-like manifestations in mice.
- Source :
- American Journal of Physiology: Lung Cellular & Molecular Physiology; Sep2018, Vol. 315 Issue 3, pL382-L386, 5p
- Publication Year :
- 2018
-
Abstract
- We have shown that cigarette smoke (CS)-induced pulmonary emphysema-like manifestations are preceded by marked suppression of the number and function of bone marrow hematopoietic progenitor cells (HPCs). To investigate whether a limited availability of HPCs may contribute to CS-induced lung injury, we used a Food and Drug Administration-approved antagonist of the interactions of stromal cell-derived factor 1 (SDF-1) with its chemokine receptor CXCR4 to promote intermittent HPC mobilization and tested its ability to limit emphysema-like injury following chronic CS. We administered AMD3100 (5mg/kg) to mice during a chronic CS exposure protocol of up to 24 wk. AMD3100 treatment did not affect either lung SDF-1 levels, which were reduced by CS, or lung inflammatory cell counts. However, AMD3100 markedly improved CS-induced bone marrow HPC suppression and significantly ameliorated emphysema-like end points, such as alveolar airspace size, lung volumes, and lung static compliance. These results suggest that antagonism of SDF-1 binding to CXCR4 is associated with protection of both bone marrow and lungs during chronic CS exposure, thus encouraging future studies of potential therapeutic benefit of AMD3100 in emphysema. [ABSTRACT FROM AUTHOR]
- Subjects :
- PULMONARY emphysema
CIGARETTE smoke
LABORATORY mice
Subjects
Details
- Language :
- English
- ISSN :
- 10400605
- Volume :
- 315
- Issue :
- 3
- Database :
- Complementary Index
- Journal :
- American Journal of Physiology: Lung Cellular & Molecular Physiology
- Publication Type :
- Academic Journal
- Accession number :
- 131585611
- Full Text :
- https://doi.org/10.1152/ajplung.00185.2018