Abstract
Gut microbiota is an essential factor in the shaping of intestinal immune system development and driving inflammation in inflammatory bowel disease (IBD). We report the effects and microbe-host interactions underlying an intervention using fine powder of eggshell membrane (ESM) against IBD. ESM attenuated lipopolysaccharide-induced inflammatory cytokine production and promoted the Caco-2 cell proliferation by up-regulating growth factors in vitro. In a murine model of dextran sodium sulphate-induced colitis, ESM significantly suppressed the disease activity index and colon shortening. These effects were associated with significant ameliorations of gene expressions of inflammatory mediators, intestinal epithelial cell proliferation, restitution-related factors and antimicrobial peptides. Multifaceted integrated omics analyses revealed improved levels of energy metabolism-related genes, proteins and metabolites. Concomitantly, cecal metagenomic information established an essential role of ESM in improving dysbiosis characterized by increasing the diversity of bacteria and decreasing absolute numbers of pathogenic bacteria such as Enterobacteriaceae and E. coli, as well as in the regulation of the expansion of Th17 cells by suppressing the overgrowth of segmented filamentous bacteria. Such modulations have functional effects on the host; i.e., repairing the epithelium, regulating energy requirements and eventually alleviating mucosal inflammation. These findings are first insights into ESM’s modulation of microbiota and IBD suppression, providing new perspectives on the prevention/treatment of IBD.
Highlights
Using antibiotics, prebiotics, probiotics or fecal microbiota transplantation[2,3,4]
The interleukin (IL)-6 concentration in the medium was significantly lower in LPS +eggshell membrane (ESM)-treated cells compared to LPS-stimulated cells alone (Fig. 1b)
The real-time reverse transcription-polymerase chain reaction (RT-PCR) results indicated the following in LPS-treated cells: the expression of genes for IL-1β were significantly down-regulated by the supplementation with ESM; the same supplementation up-regulated the cell proliferation-related factors connective tissue growth factor (CTGF) and platelet-derived growth factor alpha (PDGFA), and the potent vasoconstrictor peptide endothelin 1 (EDN1) (Fig. 1c)
Summary
Using antibiotics, prebiotics, probiotics or fecal microbiota transplantation[2,3,4]. We previously obtained nutrigenomic information from in vivo and in vitro investigations of ESM, and we observed biochemical functions of ESM that counter liver injury and fibrosis. These protective effects of ESM appear to be based on the regulation of proteins and genes that are related to the activation of hepatic stellate cells and fibrogenesis, via a potential novel modulation of the PPARγ-endothelin 1 interaction signaling pathway[8]. We found that ESM regulated the cell proliferation and restitution and ameliorated energy metabolism as well as intestinal microbiota dysbiosis We attribute these effects to altered host defense and decreased susceptibility of the host to intestinal inflammation
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