Use of senescence-accelerated mouse model in bleomycin-induced lung injury suggests that bone marrow-derived cells can alter the outcome of lung injury in aged mice

Jianguo Xu, Edilson T. Gonzalez, Smita Iyer, Valerie Mac, Ana L. Mora, Roy L. Sutliff, Alana Reed, Kenneth L. Brigham, Patricia Kelly, Mauricio Rojas

Research output: Contribution to journalArticle

62 Scopus citations


The incidence of pulmonary fibrosis increases with age. Studies from our group have implicated circulating progenitor cells, termed fibrocytes, in lung fibrosis. In this study, we investigate whether the preceding determinants of inflammation and fibrosis were augmented with aging. We compared responses to intratracheal bleomycin in senescence-accelerated prone mice (SAMP), with responses in age-matched control senescence-accelerated resistant mice (SAMR). SAMP mice demonstrated an exaggerated inflammatory response as evidenced by lung histology. Bleomycin-induced fibrosis was significantly higher in SAMP mice compared with SAMR controls. Consistent with fibrotic changes in the lung, SAMP mice expressed higher levels of transforming growth factor-β1 in the lung. Furthermore, SAMP mice showed higher numbers of fibrocytes and higher levels of stromal cell-derived factor-1 in the peripheral blood. This study provides the novel observation that apart from increases in inflammatory and fibrotic factors in response to injury, the increased mobilization of fibrocytes may be involved in age-related susceptibility to lung fibrosis.

Original languageEnglish (US)
Pages (from-to)731-739
Number of pages9
JournalJournals of Gerontology - Series A Biological Sciences and Medical Sciences
Issue number7
StatePublished - Jul 1 2009
Externally publishedYes



  • Bone marrow
  • Lung
  • Mice
  • Senescence

ASJC Scopus subject areas

  • Aging
  • Geriatrics and Gerontology

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