Ghrelin abates bacterial translocation following burn injury by improving gastric emptying

In severe burns, increased intestinal permeability facilitates bacterial translocation, resulting in systemic endotoxemia and multi^- organ failure. We investigated the role of burn-induced gastrointestinal dysmotility (BIGD) in promoting bacterial translocation following burn injury, and the protective effect of ghrelin in this process.

We assessed gastric emptying (GE%) and intestinal transit (IT by geometric center "GC") in a 60% total body surface area scald burn rat model and measured bacterial counts in mesenteric lymph nodes (MLN) and distal small intestine by colony-forming unit per gram of tissue (CFU/g). A group of animals was treated with ghrelin or saline after burn.

Scald burn was associated with a significant delay in GE (62% ± 4% vs 74% ± 4%; P = .02) and a trend of delay in intestinal transit (GC: 5.5 ± 0.1 vs 5.8 ± 0.2; P = .09). Concurrently, there was a marginal increase in small intestinal bacterial overgrowth (6 × 10⁵ vs 2 × 10⁵  CFU/g; P = .05) and significant translocation to MLN (2 × 10² vs 4 × 10¹ ; P = .03). We observed a negative correlation between GE and intestinal bacterial overgrowth (r_s  = -0.61; P = .002) and between IT and translocation (r_s  = -0.63; P = .004). Ghrelin administration significantly accelerated GE following burn injury (91% ± 3% vs 62% ± 4; P = .03), reduced small intestinal bacterial overgrowth, and completely inhibited translocation to MLN (0.0 vs 5 × 10² ; P = .01).

Burn-induced gastrointestinal dysmotility is correlated with the systemic translocation of gram-negative gut bacteria that are implicated in multiple organ failure in burn patients. Therapeutic interventions to restore BIGD are warranted (Neurogastroenterol Motil, 2012, 24, 78).