On page 929 in the 23 February 2017 issue, there is an error in Figure 1. The presence of Lactobacillus in the figure suggests that there is evidence of reduced abundance in graft-versus-host disease (GVHD) patients, which is incorrect. Therefore, the corrected Figure 1, shown below, omits Lactobacillus. The error has been corrected in the online version, which now differs from the print version.
Intestinal damage and dysbiosis linked to GVHD. Upon HCT, multiple factors such as conditioning toxicity, antibiotic treatment, and immune activation mediate GVHD. GVHD progression associates with injury to stem cell compartments along with Paneth cells (small intestine) and goblet cells. This leads to increased intestinal permeability, inflammation, and reduction of the mucus layer and antimicrobial products (eg, defensins). Antibiotic treatment and a limited amount of nutrients in the gut also promote gut dysbiosis, furthering gastrointestinal damage and disease. DC, dendritic cell; IgA, immunoglobulin A.
Intestinal damage and dysbiosis linked to GVHD. Upon HCT, multiple factors such as conditioning toxicity, antibiotic treatment, and immune activation mediate GVHD. GVHD progression associates with injury to stem cell compartments along with Paneth cells (small intestine) and goblet cells. This leads to increased intestinal permeability, inflammation, and reduction of the mucus layer and antimicrobial products (eg, defensins). Antibiotic treatment and a limited amount of nutrients in the gut also promote gut dysbiosis, furthering gastrointestinal damage and disease. DC, dendritic cell; IgA, immunoglobulin A.
