Nutrient gene interactions and the inflammatory response

The function of inflammation is to combat pathogens following injury and surgery. During the inflammatory response, muscle and adipose tissue are catabolised to provide amino acids, glucose and fatty acids, for the immune response. The liver increases acute phase protein synthesis and anti-oxidant defences are enhanced by increased glutathione synthesis. Oxidants production creates a hostile environment for pathogens. The strength of the response is modulated by pro-inflammatory and anti-inflammatory cytokines. Interleukins (IL) 1 and 6 and tumour necrosis factor-? (TNF-?), fall into the first category, and IL-10 into the second. Neuroendocrine responses occur, and heat shock proteins are produced to curtail the inflammatory response. Inflammation exerts damaging and lethal effects. High production of IL-1 and TNF-? increases mortality in cerebral malaria, meningitis and sepsis. The ratio of pro- to anti-inflammatory cytokines also result in an adverse outcome to infection. High IL-6 to IL-10, and IL-10 to TNF ratios are associated with raised mortality. IL-1, IL-6 and TNF-? also play a damaging role in inflammatory disease and atheromatous plaque development. Genotype is a key factor which influences cytokine production and the strength of the inflammatory response. TNF-?, IL-1?, IL-6 and IL-10 production is strongly influenced by single nucleotide polymorphisms (SNPs) in the promoter region of the respective genes. Cytokine gene alleles are linked to increased morbidity in a range of diseases and conditions including sepsis, diabetes mellitus and cardiovascular disease. Studies on the anti-inflammatory effect of n-3 PUFAs indicate that individual genotype may influence the efficacy of immunonutrients in controlling inflammation. To improve patient outcome a better understanding is needed, of how nutrients, such as n-3 PUFAs can be used to control the inflammatory process and how individual genotype influences the response to such immunonutrients