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Title:   Author  item
                                            Huang, Shurongitem
                                            RUTKOWSKY, JENNIFER - University Of Californiaitem
                                            SNODGRASS, RYAN - University Of Californiaitem
                                            ONO-MOORE, KIKUMI - University Of Californiaitem
                                            Schneider, Dinaitem
                                            Newman, Johnitem
                                            Adams, Seanitem
                                            Hwang, Daniel
  Submitted to: Journal of Lipid Research
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 2/1/2012
                                    Publication  Date: 7/4/2012
                                    Citation: Huang, S., Rutkowsky, J.M., Snodgrass, R.G., Ono-Moore, K., Schneider, D.A., Newman, J.W., Adams, S.H., Hwang, D.H. 2012. Saturated fatty acids activate TLR-mediated pro-inflammatory signaling pathways. Journal of Lipid Research. Epublished. DOI: 10.1194/jlr.D029546.Interpretive Summary: Toll-like receptor 4 (TLR4) and TLR2 were shown to be activated by saturated fatty acids (SFAs) but inhibited by docosahexaenoic acid (DHA). However, one report (ATVB 11:1944, 2009) suggested that SFA-induced TLR activation in cell culture systems is due to contaminants in the bovine serum albumin (BSA) or fatty acid preparation used for conjugating fatty acids. This report casted a doubt about proinflammatory effects of SFAs. Our studies herein present multiple evidence demonstrating that activation of TLR-mediated signaling pathways by SFAs is fatty acid specific effects and not due to the contaminants in BSA or fatty acid preparations.
                                Technical Abstract: Toll-like receptor 4 (TLR4) and TLR2 were shown to be activated by saturated fatty acids (SFAs) but inhibited by docosahexaenoic acid (DHA). However, one report (ATVB 11:1944, 2009) suggested that SFA-induced TLR activation in cell culture systems is due to contaminants in BSA used for conjugating fatty acids. This report cast doubt about proinflammatory effects of SFAs. Our studies herein demonstrate that sodium palmitate (C16:0) or laurate (C12:0) without BSA conjugation induced phosphorylation of JNK and ERK, and TLR target gene  expression in THP1 monocytes or RAW264.7 macropages, respectively when cultured in a low FBS (0.25%) medium. C12:0 induced NFkB activation through TLR2 dimerized with TLR1 or TLR6, and through TLR4. Since BSA was not used in these experiments, contaminants in BSA have no relevance. Unlike suspension cells (THP-1), BSA conjugation is required for C16:0 to induce TLR target gene expression in adherent cells (RAW264.7). BSA conjugated C16:0 transactivated TLR2 dimerized with TLR1 or TLR6, and through TLR4 as with C12:0. These results and additional studies with LPS sequester Polymixin B and MyD88-/- macrophages indicated that that SFA-induced activation of TLR2 or TLR4 is a fatty acid-specific effect, but not due to contaminants in BSA or fatty acid preparations.


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