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1 Division of Pulmonary, Allergy and Critical Care Medicine, United States; Center for Translational Research in the Lung, United States
2 Division of Pulmonary, Allergy and Critical Care Medicine, United States; Center for Translational Research, United States
3 Division of Pulmonary, Allergy and Critical Care Medicine, United States; Center for Translational Research, United States; McKelvey Center for Lung Transplantation, United States
4 Center for Translational Research, United States
* To whom correspondence should be addressed. E-mail: mrojas{at}emory.edu.
Bone marrow-derived mesenchymal stem cells (BMDMSCs) appear to be important in repair of the chronic lung injury caused by bleomycin in mice. To determine effects of these BMDMSCs on an acute inflammatory response, we injected C57BL/6 mice intraperitoneally with 1mg/kg endotoxin followed either by intravenous infusion of 5 x105 BMDMSCs, the same number of lung fibroblasts or an equal volume of normal saline solution. Lungs harvested 6, 24 and 48 hours and 14 days after endotoxin showed that BMDMSC administration prevented endotoxin induced lung inflammation, injury and edema. Although we were able to detect donor cells in the lungs at 1 day after endotoxin, by 14 days no donor cells were detected. BMDMSC administration suppressed the endotoxin induced increase in circulating pro-inflammatory cytokines without decreasing circulating levels of anti-inflammatory mediators. Ex vivo co-cultures of BMDMSC and lung cells from endotoxemic animals demonstrated a bilateral conversation in which lung cells stimulated proliferation and migration of stem cells and suppressed pro-inflammatory cytokine production by lung cells. We conclude that BMDMSCs decrease both the systemic and local inflammatory responses induced by endotoxin. These effects do not require either lung engraftment or differentiation of the stem cells and are due at least in part to the production of stem cell chemoattractants by the lungs and to humoral and physical interactions between stem cells and lung cells. We speculate that mobilization of this population of BMDMSCs may be a general mechanism for modulating an acute inflammatory response.
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