Lung inflammatory environments differentially alter mesenchymal stromal cell behavior

Soraia C. Abreu, Sara Rolandsson Enes, Jacob Dearborn, Meagan Goodwin, Amy Coffey, Zachary D. Borg, Claúdia C. Dos Santos, Matthew J. Wargo, Fernanda F. Cruz, Roberto Loi, Michael DeSarno, Takamuru Ashikaga, Mariana A. Antunes, Patricia R.M. Rocco, Kathleen D. Liu, Jae Woo Lee, Michael A. Matthay, David H. McKenna, Daniel J. Weiss

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


Mesenchymal stromal (stem) cells (MSCs) are increasingly demonstrated to ameliorate experimentally induced lung injuries through diseasespecific anti-inflammatory actions, thus suggesting that different in vivo inflammatory environments can influence MSC actions. To determine the effects of different representative inflammatory lung conditions, human bone marrow-derived MSCs (hMSCs) were exposed to in vitro culture conditions from bronchoalveolar lavage fluid (BALF) samples obtained from patients with either the acute respiratory distress syndrome (ARDS) or with other lung diseases including acute respiratory exacerbations of cystic fibrosis (CF) (non-ARDS). hMSCs were subsequently assessed for time- and BALF concentration- dependent effects on mRNA expression of selected pro- and anti-inflammatory mediators, and for overall patterns of gene and mRNA expression. Both common and disease-specific patterns were observed in gene expression of different hMSC mediators, notably interleukin (IL)-6. Conditioned media obtained from non-ARDS BALF-exposed hMSCs was more effective in promoting an antiinflammatory phenotype in monocytes than was conditioned media from ARDS BALF-exposed hMSCs. Neutralizing IL-6 in the conditioned media promoted generation of anti-inflammatory monocyte phenotype. This proof of concept study suggest that different lung inflammatory environments potentially can alter hMSC behaviors. Further identification of these interactions and the driving mechanisms may influence clinical use of MSCs for treating lung diseases.

Original languageEnglish (US)
Pages (from-to)L823-L831
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number6
StatePublished - 2019

Bibliographical note

Funding Information:
D. J. Weiss is supported by Cystic Fibrosis Foundation Research Grants WEISS15XX0 and WEISS16GO. S. Rolandsson Enes is supported by a Marie Curie Post-doctoral Research Fellowship (RESPIRE3) from the European Respiratory Society and the European Union’s H2020 Research and Innovation Programme (Marie Sklodowska-Curie Grant Agreement No. 713406). M. A. Matthay is supported by National Heart, Lung, and Blood Institute (NHLBI) Grants U01 HL123004 and R42 HL126456. D. H. McKenna is

Funding Information:
supported by the NHLBI PACT program, University of Minnesota, Molecular and Cellular Therapeutics, contract HHSN268201000008’.

Publisher Copyright:
© the American Physiological Society.


  • Acute respiratory distress syndrome
  • Cystic fibrosis
  • Interleukin 6
  • Lung injury
  • Mesenchymal stromal (stem) cell


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