Cytokine production of the human monocytic cell line Mono Mac 6 in comparison to mature monocytes in peripheral blood mononuclear cells
Mono Mac 6 is a human monocytic cell line with several features of mature blood monocytes such as CD 14 antigen expression, phagocytotic ability, and the functional ability to produce cytokines. This line is often used as an in vitro model to demonstrate the actions of monocytes. In our study, the production of cytokines by Mono Mac 6 cells in response to various stimulants was analyzed and compared to that of mature monocytes in peripheral blood mononuclear cells (PBMC). Interestingly, the Mono Mac 6 cells produced IL-1 alpha/beta, IL-6, and TNF-alpha after induction with the lectin phytohaemagglutinin A (PHA), mainly known as a T cell activator. The amount of cytokine release did not decrease in the presence of polymyxin B (Pmb), an inhibitor of LPS-induced effects. Kinetic studies revealed maximum cytokine levels 24h after stimulation, whereas human PBMC produced higher yields of all cytokines and enhancement was observed up to 48 hours after induction. Stimulation with the superantigen derived from the supernatant of mycoplasma arthritidis (MAS) induced expression of IL-1 beta, IL-6, and TNF-alpha, whereas staphylococcus enterotoxin B (SEB) did not induce any cytokine release. Further experiments analyzed the ability of Mono Mac 6 cells to produce IFN-alpha which is an important characteristic of mature monocytes. The cells were induced either with inactivated Newcastle Disease Virus (NDV), Sendai Virus, or the synthetic stimulus poly I:C IFN-alpha expression was not detected on the transcriptional or the protein level. In addition, no co-expression of IL-1 and IL-6 was observed in response to these stimuli. Since NDV, Sendai Virus, and poly I:C represent strong IFN-alpha inducers in peripheral blood monocytes, these data indicate that Mono Mac 6 cells lack the ability to express IFN-alpha. In conclusion, our findings show that this cell line is a potent cytokine producer, but the capacity to produce IFN is apparently deficient.
|Authors:||Neustock, P., Brand, J.M., Kruse, A., Kirchner, H.|
|Journal:||Immunobiol., 188: 293-302|
|PubMed:||Find in PubMed|