Nutrition, immune function, and inflammation: an overview.

Abstract

The collective evidence suggests that nutritional insult to both cell-mediated and humoral immunity in the presence of protein-energy malnutrition contributes to abnormalities of inflammation. The primary goal of nutritional support in inflammatory disease is to provide adequate energy and protein to meet endogenous requirements for tissue repair, IL-1 production, and restored cellular function, thus preventing secondary infection. Substrate provision should aim at improving the acute phase of injury while avoiding immune dysfunction. This goal may be achieved by altering the eicosanoid pathway toward a more regulated inflammatory state. In the context of allograft response, macrophages are central to the initiation of allosensitization by virtue of their ability to present antigen to T-cells. Activated T-cells may further modulate macrophage function by the secretion of lymphokines. Manipulation of macrophage eicosanoid production by dietary omega-3 PUFA may reduce cellular immune response. (table; see text) Nutritional support should also focus on providing essential micronutrients, with their potentially immunomodulating role, as adjunctive therapy in order to protect the host from toxic effects of free-radicals and chemicals released during inflammatory events. (Feeding regimens currently under investigation and development are presented in Table 4.) By integrating dietary immunotherapy with the use of recombinant hormones, monoclonal antibodies, and various available monokines, an optimal outcome for each patient may be achieved. However, effective application of immunotherapy to nutritional supplementation will require accurate monitoring of immune function in individual patients in order to avoid inappropriate treatment.