1. Eggshell membrane powder ameliorates intestinal inflammation by facilitating the restitution of epithelial injury and alleviating microbial dysbiosis.
- Author
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Jia H, Hanate M, Aw W, Itoh H, Saito K, Kobayashi S, Hachimura S, Fukuda S, Tomita M, Hasebe Y, and Kato H
- Subjects
- Animals, Antimicrobial Cationic Peptides metabolism, Antimicrobial Cationic Peptides therapeutic use, Caco-2 Cells, Cell Proliferation drug effects, Colitis chemically induced, Colitis pathology, Colitis prevention & control, Colitis veterinary, Dextran Sulfate toxicity, Energy Metabolism drug effects, Enterobacteriaceae drug effects, Enterobacteriaceae genetics, Humans, Interleukin-6 metabolism, Intestinal Mucosa drug effects, Lipopolysaccharides toxicity, Male, Mice, Mice, Inbred C57BL, Th17 Cells cytology, Th17 Cells drug effects, Th17 Cells metabolism, Transcriptome drug effects, Antimicrobial Cationic Peptides pharmacology, Dysbiosis, Egg Shell metabolism, Gastrointestinal Microbiome drug effects, Intestinal Mucosa metabolism
- 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.
- Published
- 2017
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