Fig. 5

MSC-dependent modulation of macrophage plasticity in IL6Rα-deficient cells. Preconditioned MSCs (acMSCs) were co-cultured with wild type macrophages or macrophages isolated from the bone marrow of IL-6Rα-deficient (IL6R-KO) mice. For differentiation toward an M1-like and M2a-like phenotype, cells were treated with 20 ng/ml IFN-ɣ + 100 ng/ml LPS (a) or 20 ng/ml IL-4 (b), respectively, for 24 h. Gene expression of IL-6, TNF-α, M2a markers (Ym-1, FIZZ1/RELMα), M2b markers (SPHK1, LIGHT), and the M2c marker MertK in macrophages was analyzed by real-time PCR. Results are representative for six to nine independent experiments and are expressed as fold change vs. expression found in macrophages. *p < 0.05, **p < 0.01 vs. gene expression found in wild type macrophages (M1 or M2) co-cultured with preconditioned MSCs (acMSCs). FIZZ1/RELMα: found in inflammatory zone 1/resistin-like molecule alpha, IL interleukin, IL-6Rα interleukin 6 receptor alpha, KO knockout, LIGHT lymphotoxin-like, exhibits inducible expression and competes with HSV glycoprotein D for herpes virus entry mediator, a receptor expressed by T lymphocytes, M macrophage, MertK tyrosine-protein kinase MER, MSCs mesenchymal stem cells, acMSCs activated, preconditioned mesenchymal stem cells, SPHK1, sphingosine kinase 1, TNF-α tumor necrosis factor alpha, Ym-1 chitinase-like protein