Intestine immune homeostasis after alcohol and burn injury

Abstract

Traumatic injury remains one of the most prevalent reasons for patients to be hospitalized. Burn injury accounts for 40,000 hospitalizations in the United States annually, resulting in a large burden on both the health and economic system and costing millions of dollars every year. The complications associated with postburn care can quickly cause life-threatening conditions including sepsis and multiple organ dysfunction and failure. In addition, alcohol intoxication at the time of burn injury has been shown to exacerbate these problems. One of the biggest reasons for the onset of these complications is the global suppression of the host immune system and increased susceptibility to infection. It has been hypothesized that infections after burn and other traumatic injury may stem from pathogenic bacteria from within the host's gastrointestinal tract. The intestine is the major reservoir of bacteria within the host, and many studies have demonstrated perturbations of the intestinal barrier after burn injury. This article reviews the findings of these studies as they pertain to changes in the intestinal immune system after alcohol and burn injury.

Figure 1. T cell differentiation into various subsets

Flow diagram of T cell differentiation into Th1, Th2, Th17, and Treg subsets under homeostatic (left) and following burn injury (right). Cytokines in red are decreased in intestinal tissues following injury, cytokines in green are increased in intestinal tissues following injury.

Figure 2. Classical T cell activation and inhibition

T cell activation (left) occurs when the T cell receptor is presented with antigen loaded onto MHC molecules expressed on antigen presenting cells. The binding of the T cell co-receptor CD28 with CD80/86 molecules on antigen presenting cells contributes to T cell activation. T cell inhibition (right) occurs when the T cell inhibitory molecules CTLA-4 binds to CD80/86 on antigen presenting cells.