Transplantation of human placenta mesenchymal stem cells reduces the level of inflammatory factors in lung tissues of mice with acute lung injury

: Objective To investigate the influence of human placenta mesenchymal stem cells (hPMSCs) on the expression levels of inflammatory factors in the lung tissues of lipopolysaccharide (LPS)-induced acute lung injury (ALI) mice. Methods Six-week-old healthy C57BL/6 male mice were randomly divided into control group, ALI model group and hPMSC-treated group, with 8 mice in each group. LPS was trickled in ALI model group by the trachea. The hPMSC-treated mice were injected with hPMSCs by tail vein at 12 hours after administration of LPS. The control group was managed with the corresponding dose of normal saline. The surface markers of hPMSCs were identificated by flow cytometry. The mice were sacrificed after 24 hours, and the histopathological changes of lung tissues were detected by HE staining before and after injection of hPMSCs. The dry to wet mass ratio (W/D) and the myeloperoxidase (MPO) activity of the lung tissues were tested, and the levels of inflammatory factors in bronchoalveolar lavage fluid (BALF) were measured by ELISA, including tumor necrosis factor (TNF-α), interleukin-1 (IL-1) and interleukin-6 (IL-6). Results Phenotypic identification of hPMSCs showed the positive expression for CD105, CD90 and CD73, but negative expression for CD14, CD34, CD45. Compared with the control group, the pathological injury of the lung tissues was severe in the ALI model group, the W/D ratio and MPO activity in the lung tissues increased, and the levels of TNF-α, IL-1, and IL-6 in the BALF were significantly elevated. Compared with the ALI model group, the treatment with hPMSCs alleviated the lung pathological damage, decreased the W/D ratio and MPO activity in the lung tissues, and down-regulated the expressions of TNF-α, IL-1 and IL-6 in the BALF. Conclusion Treatment with hPMSCs can reduce the levels of inflammatory cytokines in the lung tissues and attenuate LPS-induced ALI.