Well, I guess the question is what you want. If you want to see how monocytes react to viral infection, you are fine. If you want to see how macrophages react to viral infection, you need to use PMA and differentiate the THP1. If you want to see if your virus forces your monocytes to differentiate to macrophages (like some groups have shown) you should not differentiate with any PMA.
Phospholipid transfer protein (PLTP) plays an important role in regulation of inflammation. Previously published studies have shown that PLTP binds, transfers and neutralizes bacterial lipopolysa-ccharides. In the current study we tested the hypothesis that PLTP can also regulate anti-inflammatory pathways in macrophages. Incubation of macrophage-like differentiated THP1 cells and human monocyte-derived macrophages with wild-type PLTP in the presence or absence of tumor necrosis factor alpha (TNFα) or interferon gamma (IFNγ) significantly increased nuclear levels of active signal transducer and activator of transcription 3, pSTAT3Tyr705 (p < 0.01). Similar results were obtained in the presence of a PLTP mutant without lipid transfer activity (PLTPM159E), suggesting that PLTP-mediated lipid transfer is not required for activation of the STAT3 pathway. Inhibition of ABCA1 by chemical inhibitor, glyburide, as well as ABCA1 RNA inhibition, reversed the observed PLTP-mediated activation of STAT3. In addition, PLTP reduced nuclear levels of active nuclear factor kappa-B (NFκB) p65 and secretion of pro-inflammatory cytokines in conditioned media of differentiated THP1 cells and human monocyte-derived macrophages. Our data suggest that PLTP has anti-inflammatory capabilities in macrophages.
References
W.DongaG.Wolfbauer C.Tang J.J.Albers. PLTP regulates STAT3 and NFκB in differentiated THP1 cells and human monocyte-derived macrophages.Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 1813( 10), 2011, Pages 1917-1924