Adipose-immune cell cross-talks in two pig lines divergently selected for feed efficiency - Part 1

Adipose tissue is now recognized as an endocrine organ with a role in organ cross-talk. It produces a number of factors including inflammatory cytokines such as Tumor Necrosis Factor α (TNF-α). This factor regulates also adipocyte differentiation and adipokine secretion. The aim of this study was to determine if different levels of immune stimulation influenced the features of adipose tissue cells in two lines of pigs, divergently selected for residual feed intake (RFI), a measure of feed efficiency. Growing pigs (n=24) of low (RFI-) or high (RFI+) RFI were reared in clean or dirty housing conditions for 6 weeks, to obtain healthy and chronically inflamed animals, respectively. After subcutaneous adipose tissue collection, adipocytes and cells of the stromal vascular fraction (SVF) were isolated. Gene expression levels were determined in freshly isolated adipocytes and SVF cells. TNF-α, Toll-Like Receptor (TLR) 2 and 4 mRNA were expressed in SVF cells but were not detected in adipocytes. Levels of TLR2 were higher (P<0.05) in RFI+ than in RFI- pigs in both housing conditions. The IL6 gene was expressed in both adipocytes and SVF cells with no difference between the experimental groups. SVF cells were cultured in differentiation medium in the absence or presence of TNF-α (1 and 10 ng/ml). TNF-α inhibited the accumulation of lipid droplets in SVF cells of the different groups, indicating an impaired differentiation (P<0.05). Analysis of gene expression in differentiated cells demonstrated that TNF-α impaired Malic Enzyme (ME) (P<0.05). In conclusion, the expression of the TNF-α gene in SVF cells and the response of these cells in culture to TNF-α did not differ between healthy and chronic inflamed animals. The finding of a higher TLR2 expression in RFI+ suggests difference in the immune response between the two pig lines that needs to be further investigated. Research has received funding from the EU FP7 program (PROHEALTH, grant agreement no. 613574).