AMD3100 ameliorates cigarette smoke-induced emphysema-like manifestations in mice

Daria Barwinska, Houssam Oueini, Christophe Poirier, Marjorie E. Albrecht, Natalia V. Bogatcheva, Matthew J. Justice, Jacob Saliba, Kelly S. Schweitzer, Hal E. Broxmeyer, Keith L. March, Irina Petrache

Research output: Contribution to journalArticle

5 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)L382-L386
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number3
StatePublished - Sep 2018


  • Bone marrow
  • COPD
  • Emphysema
  • Lung treatment

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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