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Background  The intestinal barrier integrity is crucial for maintaining intestinal homeostasis, and the mechanisms of intestinal barrier disruption induced by burn injury remain obscure. This study was aimed to investigate the changes of intestinal microbiota and barrier function in burned mice to further comprehend the mechanisms of burn-induced intestinal barrier dysfunction.    Methods  Samples were from mice inflicted with 30% total body surface area (TBSA) full-thickness burns. The intestinal permeability, tight junction proteins expressions, zonula occludens-1 (ZO-1) localization, inflammatory cytokines expressions, and short-chain fatty acids (SCFAs) contents were determined. The microbial community was assessed via 16S rDNA Illumina sequencing.    Results  The intestinal permeability was increased after severe burn injury, peaking at 6 h post-burn, with approximately 20-folds of the control ( p  &lt; 0.001). The expression of tight junction proteins (ZO-1, occludin, claudin-1, and claudin-2) was significantly altered ( p  &lt; 0.05). The ZO-1 morphology was dramatically changed following burn injury. The fecal SCFAs’ contents (acetate, propionate, butyrate, isobutyrate, and isovalerate) were noticeably declined after burn injury ( p  &lt; 0.05). The expressions of pro-inflammatory cytokines (interleukin (IL)-1β and IL-6) in ileal mucosa were increased, whereas the expressions of anti-inflammatory cytokines (IL-4 and IL-13) were decreased following burn injury ( p  &lt; 0.05). In addition, burned mice showed an alteration of intestinal microbial community, such as decreased diversity, reduced  Bacteroidetes  abundance, and increased  Firmicutes  abundance.    Conclusions  The severe burn-induced intestinal barrier dysfunction is along with the alterations of microbial community.    Electronic supplementary material  The online version of this article (10.1186/s41038-019-0156-1) contains supplementary material, which is available to authorized users.

Severe burn injury alters intestinal microbiota composition and impairs intestinal barrier in mice