Effect of prostate cancer cell line supernatant on functional polarization in macrophages

Bratisl Lek Listy. 2018;119(8):516-521. doi: 10.4149/BLL_2018_095.

Abstract

Objectives: We aimed on effect of supernatant derived from prostate cancer cell line PC-3 on M1/M2 functional polarization in macrophages.

Background: Cytokines play an important role in carcinogenesis. Most of them are produced by macrophages. Macrophages are divided into groups M1 or M2. Classical phenotype macrophages M1 support pro-inflammatory effects and produce pro-inflammatory cytokines, such as interleukin 6 (IL-6), interleukin 12 (IL-12), tumor necrosis factor α (TNF-α). Macrophages exhibiting a phenotype M2 secrete anti-inflammatory cytokines, e. g. interleukin 10 (IL-10), transforming growth factor β (TGF-β).

Methods: Peripheral blood monocytes were cultivated for 7 days and during this time went through a differentiation into macrophages. Macrophages were stimulated for 24 hours by lipopolysaccharide (LPS) as a positive control and cultivated with supernatant for another 24 hours.

Results: Macrophages cultivated without LPS and without supernatant were used as negative control. Relative expression of IL-6, IL-10, IL-12 and TNF-α was measured by Quantitative real-time PCR. Expression of pro-inflammatory cytokines was lower in macrophages with supernatant compared to positive control.

Conclusion: Expression of pro-inflammatory cytokines was lower in macrophages with supernatant (MΦ+sup) compared to positive control (MΦ+LPS). Effect of the supernatant on expression of IL-6, IL-10, IL-12 and TNF-α was not confirmed (Tab. 1, Fig. 5, Ref. 15).

Keywords: cancer; macrophages cytokines.; prostate; supernatant.

MeSH terms

  • Animals
  • Cell Differentiation / drug effects*
  • Cell Line
  • Cytokines / genetics
  • Cytokines / metabolism*
  • Humans
  • Interleukin-10 / genetics
  • Interleukin-10 / metabolism*
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • Lipopolysaccharides / pharmacology*
  • Macrophages / drug effects*
  • Macrophages / metabolism
  • Male
  • Prostatic Neoplasms
  • Real-Time Polymerase Chain Reaction
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Cytokines
  • IL10 protein, human
  • Interleukin-6
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Interleukin-10