Nutrition, Immune Function, and Inflammation: an overview

Abstract

The account of acute inflammation is one of the classical clinical descriptions in medicine. However, those early physicians describing Rubor et tumor cum calor et dolore (Celsus in 50 BC) could hardly have imagined the complexity of the events that they were observing.In a healthy individual, the response to tissue injury and infection is rapid and efficient, with resolution occurring before involvement of the specific immune system. However, when the inflammatory stimulus is overwhelming, or if the patient is already malnourished or chronically ill, a series of inter-related events are set in motion. Among these are the interaction of immune cells, phagocytes and release of powerful cytokines that affect the utilization of nutritional substrates in the body. Moreover, antigen processed by macrophages is presented to lymphocytes, thus eliciting a specific immune response.The present paper summarizes our present understanding of the pathophysiology of inflammation and explores the objectives for nutritional support in the presence of immunodysfunction. The rationale for adjunctive nutritional support is explained, and modified regimens, tailored both to provide metabolic substrates and to enhance immunity to disease, are given. Pathophysiology of the inflammatory responseThe immune system is phylogenetically separated into innate or non-specific immunity and the adaptive or specific immune system. While understanding that both processes are often working together, events in each system will be considered individually at a cellular and molecular level.Non-specific immunity. Tissue injury leads to release of Hageman factor (XIIa-XII) and to the degranulation of tissue mast cells. Factor XI1 initiates the process, causing complement activation and bradykinin production locally. Micro-organisms and endotoxin may also trigger this pathway, directly activate complement, or cause mast cell degranulation ( Fig. 1) (Schlesinger, 1975). This mechanism ensures the presence of inflammatory mediators such as the complement factors C3a and C5a, bradykinin, and histamine. Damaged cell membranes release products of arachidonic acid (AA) metabolism, such as prostaglandins (PG) and leukotrienes (LT) (Goetzl, 1981), both of which are eicosanoids having important mediating functions in acute inflammation. The net effect is to increase vascular pernieability, which causes the accumulation of acute-phase at https://www.cambridge.org/core/terms. https://doi

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