期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 317, 期 6, 页码 L823-L831出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00263.2019
关键词
acute respiratory distress syndrome; cystic fibrosis; interleukin 6; lung injury; mesenchymal stromal (stem) cell
资金
- Cystic Fibrosis Foundation [WEISS15XX0, WEISS16GO]
- Marie Curie Post-doctoral Research Fellowship (RESPIRE3) from the European Respiratory Society
- European Union [713406]
- National Heart, Lung, and Blood Institute (NHLBI) [U01 HL123004, R42 HL126456]
- NHLBI PACT program, University of Minnesota, Molecular and Cellular Therapeutics [HHSN268201000008]
Mesenchymal stromal (stem) cells (MSCs) are increasingly demonstrated to ameliorate experimentally induced lung injuries through disease-specific 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 anti-inflammatory 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.
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