s were performed comparing separately the higher versus lower n 3 LC PUFA families at each total lipid level, i. e. LH LL and HH HL. A Venn diagram contrasting the two t test significant lists was then per formed and when analyzing the genes that were similarly affected by n 3 LC PUFA contents at both higher and lower total lipid Imatinib Mesylate purchase level, a similar preponderance of immune response genes was observed. Finally, examination of the fold changes of immune related genes, indicating magnitude of effects, between families with higher and lower contents of n 3 LC PUFA at either higher or lower total lipid levels, showed no clear evidence of the effect being more marked for the high lipid comparison, which is what would be expected if results were caused simply by inclu sion of family HH in the transcriptomic analysis.
Hence, there is evidence to suggest that there may be some correlation between flesh n 3 LC PUFA contents and immune response in the families analysed. An anti inflammatory role of n 3 LC PUFA is well established in mammals and fish. Immune cells are typically rich in arachidonic acid, the precursor for eicosa noids with a pro inflammatory action, whereas EPA and DHA give rise to eicosanoids that are less biologically active, as well as to resolvins and protectins presenting anti inflammatory properties. Higher incorporation of n 3 LC PUFA in biological membranes of immune cells can modulate immune responses in several ways.
They alter the production of inflammatory eicosanoid mediators of which they are precursors, directly affect the organization and properties of the immune cell membranes with effects on signalling pathways, phagocytic capacity and antigen presenting capability, and activate transcription of various genes involved in inflammatory responses. Therefore, families with higher tissue levels of n 3 LC PUFA may show differ ential expression of immune response and inflammation related genes, as well as of genes involved in signalling and regulation of transcription. Furthermore, although liver is chiefly a metabolic organ, it has other physiological GSK-3 functions including removal of pathogens and antigens from the blood and modulation of immune responses, as well as the produc tion of inflammatory mediators.
Related to sellckchem the above, microarray analysis revealed the presence of several genes that intervene in eicosanoid syn thesis and metabolism including phospholipase A2, arachidonate 5 lipoxygenase, thromboxane A synthase, prostaglandin I2 synthase and 15 hydroxyprostaglandin dehydrogenase. However, RT qPCR only confirmed up regulation of hepatic alox5 in families presenting higher flesh n 3 LC PUFA and, given that alox5 acts on LC PUFA of both n 3 and n 6 series and that ARA levels generally accompanied the n 3 LC PUFA phenotype, it cannot be ascertained whether this transcript was responding to higher levels of membrane ARA or EPA and hence if it would result in increased pro inflammatory 4 series, or less potent 5 series, leukotriene