Table 1.

Effect of the intestinal microbiota on GVHD.

Host	Outcome	Possible mechanisms	Refs.
Mouse	Oral administration of Lactobacillus rhamnosus GG (LGG) before and after transplantation results in improved survival and reduced aGVHD	Mice treated with LGG have a reduced translocation of enteric bacteria	[17]
Mouse	Loss of physiologic diversity among the intestinal microbiota and the overwhelming expansion of Escherichia coli which caused septicemia	Paneth cells are targeted by GVHD, resulting in marked reduction in the expression of α-defensins	[18]
Mouse	Loss of overall diversity of gut microbiota. Eliminating Lactobacillales from the mice before BMT aggravated GVHD, whereas reintroducing Lactobacillus johnsonii mediated significant protection against GVHD	L. johnsonii reduced GVHD severity by prevention of Enterococcus expansion	[19]
Mouse	Increased bacterial translocation and serum lipopolysaccharide (LPS) levels were detected after TBI	Neutrophil granulocytes recruited upon translocation of intestinal bacteria enhance GVHD via tissue damage	[33]
Mouse	The inflammatory responses in intestinal GVHD (iGVHD) were accompanied by gut flora shifts towards Enterobacteria, Enterococci, and Bacteroides/Prevotella spp.	iGVHD development is mediated by MyD88/TLR9-dependent bacterial sensing	[34]
Human	Successful total gastrointestinal decontamination (GID) of the graft recipient prevents moderate to severe acute GVHD	Prevention of intestinal microorganisms translocation	[35]
Human	After transplantation, a relative shift toward Enterococci was observed, especially in patients that developed subsequently or suffered from active GI GVHD	Early microbiome shifts may affect intestinal inflammation in the setting of allogeneic SCT	[31]
Human	Mortality outcomes were significantly worse in patients with lower intestinal tract bacterial diversity	Intestinal microbiota may be an important factor in the success or failure in allo-HSCT	[32]