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Expanded endothelial progenitor cells mitigate lung injury in septic mice
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Previous issue date: 2015Technische Universität Dresden. University Hospital Dresden. Department of Anesthesiology and Intensive Care Medicine. Dredesm Germany / Universidade Federal do Rio de Janeiro. Centro de Ciências da Saúde. Instituto de Biofísica Carlos Chagas Filho (IBCCF). Laboratório de Investigação Pulmonar. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Centro de Ciências da Saúde. Instituto de Biofísica Carlos Chagas Filho (IBCCF). Laboratório de Investigação Pulmonar. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Centro de Ciências da Saúde. Instituto de Biofísica Carlos Chagas Filho (IBCCF). Laboratório de Investigação Pulmonar. Rio de Janeiro, RJ, BrasilUniversidade Federal do Rio de Janeiro. Centro de Ciências da Saúde. Instituto de Biofísica Carlos Chagas Filho (IBCCF). Laboratório de Investigação Pulmonar. Rio de Janeiro, RJ, BrasilPontifícia Universidade Católica do Paraná. Centro de Tecnologia Celular. Curitiba, PR, Brasil.Universidade Federal do Rio de Janeiro. Centro de Ciências da Saúde. Instituto de Biofísica Carlos Chagas Filho (IBCCF). Laboratório de Investigação Pulmonar. Rio de Janeiro, RJ, BrasilUniversidade Federal do Rio de Janeiro. Centro de Ciências da Saúde. Instituto de Biofísica Carlos Chagas Filho (IBCCF). Laboratório de Investigação Pulmonar. Rio de Janeiro, RJ, BrasilPontifícia Universidade Católica do Paraná. Centro de Tecnologia Celular. Curitiba, PR, Brasil.Technische Universität Dresden. University Hospital Dresden. Department of Anesthesiology and Intensive Care Medicine. Dredesm Germany.Universidade Federal do Rio de Janeiro. Centro de Ciências da Saúde. Instituto de Biofísica Carlos Chagas Filho (IBCCF). Laboratório de Investigação Pulmonar. Rio de Janeiro, RJ, Brasil.Endothelial progenitor cells (EPCs) improve survival and reduce organ failure in cecal ligation and puncture-induced
sepsis; however, expanded EPCs may represent an even better approach for vascular repair. To date, no study has
compared the effects of non-expanded EPCs (EPC-NEXP) with those of expanded EPCs (EPC-EXP) and mesenchymal
stromal cells of human (MSC-HUMAN) and mouse (MSC-MICE) origin in experimental sepsis. One day after cecal
ligation and puncture sepsis induction, BALB/c mice were randomized to receive saline, EPC-EXP, EPC-NEXP,
MSC-HUMAN or MSC-MICE (1 × 105
) intravenously. EPC-EXP, EPC-NEXP, MSC-HUMAN, and MSC-MICE displayed
differences in phenotypic characterization. On days 1 and 3, cecal ligation and puncture mice showed decreased
survival rate, and increased elastance, diffuse alveolar damage, and levels of interleukin (IL)-1β, IL-6, IL-10, tumor
necrosis factor-α, vascular endothelial growth factor, and platelet-derived growth factor in lung tissue. EPC-EXP and
MSC-HUMAN had reduced elastance, diffuse alveolar damage, and platelet-derived growth factor compared to
no-cell treatment. Tumor necrosis factor-α levels decreased in the EPC-EXP, MSC-HUMAN, and MSC-MICE groups.
IL-1β levels decreased in the EPC-EXP group, while IL-10 decreased in the MSC-MICE. IL-6 levels decreased both in
the EPC-EXP and MSC-MICE groups. Vascular endothelial growth factor levels were reduced regardless of therapy. In
conclusion, EPC-EXP and MSC-HUMAN yielded better lung function and reduced histologic damage in septic mice