Metabolic Effects of Immune Response Mediators

When the organism is stressed by an injury, infection or illness, the daily swing of insulin- and glucagon-mediated metabolic shifts between fed and fasted states is disturbed. The organ system charged with recognising and responding to an injury is the immune system, which has the capacity to radically change body protein and energy metabolism and thus body composition [5]. The antigen-presenting cell (APC) of the immune system is typically a macrophage, tissue monocyte or skin dendritic cell. The APC contacts an antigen, phagocytoses it, processes an antigenic determinant, and brings it to its surface in an HLA-restricted manner in order to trigger an immune response. This immune response requires both the presence of a specific epitope from the antigen and the elaboration of one or more non-specific signals, chiefly via secretion of the cytokine IL-1. IL-1 secretion triggers activation of T cells and other portions of the immune response. The subsequent APC-initiated signals include the elaboration of TNF-a and, later, production of IL-6. These three cytokines (IL-1, TNF-a and IL-6) are currently thought to play the most important role in the development of the acute-phase metabolic response, which parallels the acute-phase immune response. Because there are receptors for these cytokines on every cell in the body except red blood cells, these cytokines have profound effects on the hormones that govern metabolism as well as acting directly on the metabolic target organs such as muscle, liver, gut and brain [9]. The result is an increase in resting energy expenditure, a net export of amino acids from muscle to liver, an increase in gluconeogenesis, and a marked shift in liver protein synthesis away from albumin and towards production of acute-phase proteins such as fibrinogen and C-reactive protein [10].

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