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Archive > Volume 21 Issue 3 > 2014,21(3):251-256. DOI:10.3872/j.issn.1007-385X.2014.03.003 Prev Next
Basic Research
Re-polarization of tumor-associated macrophages to M1 macrophages induced by bacteriophage T4
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Abstract:
To analyse T4 phage-induced M1 re-polarization of tumor-associated M2 type macrophages, and to evaluate the ability of re-polarized M1 macrophages on apoptosis and metastasis of mouse Lewis lung cancer cells in vitro. Methods: Mouse macrophage RAW264.7 cells were induced into M2 type macrophages by interleukin-4 (IL-4), which were subsequently induced to re-polarize with T4-bacteriophage. In both IL-4-induced M2 macrophages and T4 repolariezed-macrophages, mRNA levels of 〖STBX〗IL-12, TNF-α, Arg-1, TGF-β, IL-10〖STBZ〗 and iNOS were analyzed by Real-time PCR, and protein levels of iNOS and Arg-1 were determined by Western blotting. The effect of T4-phage-induced re-polarization on the apoptosis and metastasis of Lewis lung cancer cells were evaluated by the flow cytometry and transwell assays, respectively. Results: RAW264.7 cells were successfully induced into an M2 phenotype with a significant increase in mRNA levels of 〖STBX〗Arg-1〖STBZ〗 and 〖STBX〗IL-10〖STBZ〗 (161.2 and 120.3 folds, respectively), together with a significant decrease in iNOS and 〖STBX〗IL-12〖STBZ〗 mRNA levels (3.3 and 7.8 folds, respectively). Both wild-type and the soc-hoc-T4 bacteriophages effectively induce M1 re-polarization of M2 type macrophages, but the induction activity of the soc-hoc-T4 phages was significantly stronger than that of the wild-type (P<0.05). Both wild-type and polarized M1 type macrophages more effectively induced apoptotic cell death ([35.3±2.44]%, [39.1±2.08]% vs [4.68±0.56]%, P<0.01) and suppressed the invasive capability in Lewis lung cancer cells ([43.8±7.51]%, [23.2±4.33]% vs [177.5±12.33]%, P<0.01), as compared with M2 macrophages. Conclusion: T4 bacteriophages can induce M1 re-polarization of M2 type macrophages, which results in an increase in apoptotic cell death and a decrease in invasive activity in Lewis lung cancer cells in vitro.
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Project Supported:
Project supported by the National Natural Science Foundation of China（No. 81001028）
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