OBJECTIVETo compare the modulatory effects of human amniotic epithelial cells (H-AECs), human amniotic mesenchymal cell (HA-MSCs), umbilical mesenchymal cells (UC-MSCs) on the inflammatory status of lipopolysaccharide (LPS)-induced RAW264.7 cells.

METHODSRAW264.7 cells stimulated with LPS were co-cultured with H-AECs, HA-MSCs, or UC-MSCs or cultured in conditioned media of the 3 stem cells to assess the changes of the inflammatory status of RAW264.7 cells. The migration ability, nitric oxide concentration, and expressions of the pro-inflammatory and anti-inflammatory genes, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNFα), and inducible nitric oxide synthase (NOS-2) of M1 macrophages, and Arg-1, CD206, and CD36 of M2 macrophages, were detected in the co-cultures.

RESULTSCompared with the control macrophages, RAW264.7 cells cultured in the conditioned media of H-AECs, HA-MSCs, and UC-MSCs all showed significantly lowered migration abilities (P<0.05). Co-culture with H-AECs, but not the other two stem cells, resulted in a significant reduction of NO production (P<0.05) and significant down-regulation of IL-1β, TNFα, NOS-2, and INFβ expressions in RAW264.7 cells; co-culture with HA-MSCs and UC-MSCs only caused a down-regulation of INFβ mRNA expression. In all the 3 RAW264.7 and stem cell co-cultures, the expressions of the inflammation related genes including Arg-1, CD206, and CD36 were up-regulated significantly.

CONCLUSIONH-AECs, HA-MSCs, and UC-MSCs can all prevent RAW264.7 cells from differentiating into M2 macrophages, but their effects and mechanisms are different from one another.