IL-10 promotes development of acute respiratory distress syndrome via inhibiting differentiation of bone marrow stem cells to alveolar type 2 epithelial cells.

ABSTRACT

OBJECTIVE: To explore whether interleukin-10 (IL-10) could promote the development of acute respiratory distress syndrome (ARDS) via inhibiting differentiation of bone marrow stem cells (BMSCs) to alveolar type 2 (AT II) epithelial cells. PATIENTS AND METHODS: 25 ARDS (acute respiratory distress syndrome) patients admitted in our hospital from December 2015 to February 2018 were enrolled. Meanwhile, 25 healthy controls in the same period were selected as control group. Serum level of IL-10 in each subject was detected via ELISA (enzyme-linked immunosorbent assay). BMSCs were isolated and cultured, followed by identification of surface antigens and morphology observation using flow cytometry. For in vitro experiments, expression levels of AT II-related genes induced with or without IL-10 were detected by qRT-PCR (quantitative Real-time polymerase chain reaction) and Western blot, respectively. The culture medium of BMSCs induced with or without IL-10 was collected for detecting expression levels of interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) by ELISA. RESULTS: IL-10 was overexpressed in ARDS patients than that of healthy controls. Primary BMSCs were elongated after culturing for 1-3 days. Negative-antigen CD34 (4.32%) and positive-antigen (99.87%) on the surface of BMSCs were identified by flow cytometry. Both mRNA and protein expressions of AT II-related genes increased in a time-dependent manner. ELISA results showed that IL-10 level in cell supernatant decreased with the prolongation of induction days. Moreover, IL-10 intervention downregulated the expressions of AT II-related genes. CONCLUSIONS: IL-10 promotes ARDS development via inhibiting cell differentiation of BMSCs to AT II.