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Host | Outcome | Possible mechanisms | Refs. |
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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] |
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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] |
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Human | Successful total gastrointestinal decontamination (GID) of the graft recipient prevents moderate to severe acute GVHD | Prevention of intestinal microorganisms translocation | [35] |
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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] |
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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] |
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