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粘蛋白通过增强精氨酸代谢促进亚精胺积累缓解结肠屏障功能障碍。

Mucin alleviates colonic barrier dysfunction by promoting spermine accumulation through enhanced arginine metabolism in .

机构信息

State Key Laboratory of Animal Nutrition and Feeding, College of Animal Science and Technology, China Agricultural University, Beijing, China.

Key Laboratory of Feed Biotechnology of the Ministry of Agriculture and Rural Affairs, Institute of Feed Research, Chinese Academy of Agricultural Sciences, Beijing, China.

出版信息

mSystems. 2024 May 16;9(5):e0024624. doi: 10.1128/msystems.00246-24. Epub 2024 Apr 2.

Abstract

UNLABELLED

Dietary fiber deprivation is linked to probiotic extinction, mucus barrier dysbiosis, and the overgrowth of mucin-degrading bacteria. However, whether and how mucin could rescue fiber deprivation-induced intestinal barrier defects remains largely unexplored. Here, we sought to investigate the potential role and mechanism by which exogenous mucin maintains the gut barrier function. The results showed that dietary mucin alleviated fiber deprivation-induced disruption of colonic barrier integrity and reduced spermine production . Importantly, we highlighted that microbial-derived spermine production, but not host-produced spermine, increased significantly after mucin supplementation, with a positive association with upgraded colonic abundance. After employing an model, the microbial-derived spermine was consistently dominated by both mucin and spp. Furthermore, was identified as an essential spermine-producing spp., and this isolated strain was responsible for spermine accumulation, especially after adhering to mucin . Specifically, the mucin-supplemented bacterial supernatant of was verified to promote intestinal barrier functions through the increased spermine production with a dependence on enhanced arginine metabolism. Overall, these findings collectively provide evidence that mucin-modulated microbial arginine metabolism bridged the interplay between microbes and gut barrier function, illustrating possible implications for host gut health.

IMPORTANCE

Microbial metabolites like short-chain fatty acids produced by dietary fiber fermentation have been demonstrated to have beneficial effects on intestinal health. However, it is essential to acknowledge that certain amino acids entering the colon can be metabolized by microorganisms to produce polyamines. The polyamines can promote the renewal of intestinal epithelial cell and maintain host-microbe homeostasis. Our study highlighted the specific enrichment by mucin on promoting the arginine metabolism in to produce spermine, suggesting that microbial-derived polyamines support a significant enhancement on the goblet cell proliferation and barrier function.

摘要

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膳食纤维的缺乏与益生菌的灭绝、黏液屏障失调以及黏蛋白降解菌的过度生长有关。然而,黏蛋白是否以及如何能挽救膳食纤维缺乏引起的肠道屏障缺陷在很大程度上仍未得到探索。在这里,我们试图研究外源性黏蛋白维持肠道屏障功能的潜在作用和机制。结果表明,膳食纤维中的黏蛋白缓解了纤维剥夺引起的结肠屏障完整性的破坏,并减少了精胺的产生。重要的是,我们强调微生物衍生的精胺产生,而不是宿主产生的精胺,在黏蛋白补充后显著增加,与升级的结肠丰度呈正相关。在使用无菌模型后,微生物衍生的精胺一直由黏蛋白和 spp. 共同主导。此外,被鉴定为产生精胺的必需 spp.,并且这种分离株负责精胺的积累,尤其是在黏附于黏蛋白后。具体来说,黏蛋白补充的 细菌上清液被证实通过增加精胺的产生来促进肠道屏障功能,这依赖于增强的精氨酸代谢。总的来说,这些发现共同提供了证据,证明黏蛋白调节的微生物精氨酸代谢桥接了微生物和肠道屏障功能之间的相互作用,说明了对宿主肠道健康的可能影响。

重要的是

膳食纤维发酵产生的微生物代谢产物,如短链脂肪酸,已被证明对肠道健康有益。然而,必须承认,进入结肠的某些氨基酸可以被微生物代谢产生多胺。多胺可以促进肠上皮细胞的更新,维持宿主-微生物的平衡。我们的研究强调了黏蛋白对促进 中精氨酸代谢产生精胺的特定富集,表明微生物衍生的多胺支持杯状细胞增殖和屏障功能的显著增强。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/594b/11097634/e08874c11840/msystems.00246-24.f001.jpg

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