The paper below discusses systemic responses to burn injury including gastrointestinal response. The similarity between Crohn’s inflammatory response and the inflammatory response following gastrointestinal burn injury is not just striking, it is essentially identical!

Until Crohn’s researchers begin to consider something beyond autoimmunity as the cause of inflammation in Crohn’s guts, they will never make a breakthrough.

Adynamic ileus, gastric dilatation, increased gastric secretion and ulcer incidence, gastrointestinal hemorrhage and local and general distribution of the blood flow with a decrease of mesenteric blood flow are among the effects of thermal injury on the gastrointestinal system (53). A decrease in mesenteric blood flow has been described in a number of burn and smoke inhalation animal models, even in the absence of any evidence of inadequate systemic perfusion (54). The effect of acute burn trauma, produced by hot water scalding in the rat, has demonstrated that there is decreased nutrient absorption (glucose, calcium and amino acids) and DNA synthesis in the small intestine (55). The burn patient has been found to have a high incidence of ulcers. Erosion of the stomach lining and duodenum has been demonstrated in 86% of major burn patients within 72 h of injury, with more than 40% of patients having gastrointestinal bleeding (56).

In addition, the process of increased bacterial translocation and macromolecular leak have been well documented after burn injury, being evident in humans as well (57- 60). Intestinal ischemia resulting from decreased splanchnic blood flow may activate the neutrophils and tissue-bound enzymes such as xanthine oxidase and these factors destroy the gut mucosal barrier and result in bacterial translocation. These data indicate an early postburn gut barrier leak after the burn, which may be the source of circulating endotoxin (61). Endotoxin, a lipopolysaccharide derived from the outer membrane of Gram-negative bacteria, translocates across the gastrointestinal tract barrier within 1 h of thermal injury (62). Although the burn wound is initially sterile, plasma endotoxin concentration reaches a peak at 12 h and 4 days postburn (63). Endotoxins are potent activators of the macrophages and neutrophils. This leads to the release of massive amounts of oxidants, arachidonic acid metabolites and proteases, which cause further local and systemic inflammation in burn-induced tissue damage.
Source: http://journals.tubitak.gov.tr/medical/issues/sag-04-34-4/sag-34-4-1-0405-1.pdf