Abstract

BackgroundCalorie restriction (CR), which has a potent anti-inflammaging effect, has been demonstrated to induce dramatic changes in the gut microbiota. Whether the modulated gut microbiota contributes to the attenuation of inflammation during CR is unknown, as are the members of the microbial community that may be key mediators of this process.ResultsHere, we report that a unique Lactobacillus-predominated microbial community was rapidly attained in mice within 2 weeks of CR, which decreased the levels of circulating microbial antigens and systemic inflammatory markers such as tumour necrosis factor alpha (TNF-α). Lactobacillus murinus CR147, an isolate in the most abundant operational taxonomic unit (OTU) enriched by CR, downregulated interleukin-8 production in TNF-α-stimulated Caco-2 cells and significantly increased the lifespan and the brood size of the nematode Caenorhabditis elegans. In gnotobiotic mice colonized with the gut microbiota from old mice, this strain decreased their intestinal permeability and serum endotoxin load, consequently attenuating the inflammation induced by the old microbiota.ConclusionsOur study demonstrated that a strain of Lactobacillus murinus was promoted in CR mice and causatively contributed to the attenuation of ageing-associated inflammation.

Highlights

  • Calorie restriction (CR), which has a potent anti-inflammaging effect, has been demonstrated to induce dramatic changes in the gut microbiota

  • We report a unique Lactobacillus murinusdominated microbial community that was rapidly attained in mice within 2 weeks of CR, which decreased the levels of circulating microbial antigens and marker of systemic inflammation

  • Short-term calorie restriction improves metabolic health and alters the gut microbiota in mice To observe the effect of short-term CR on mice, we randomly assigned mice into two groups: the first group received a normal chow diet ad libitum (NC group), while the second was fed 70% of the ad libitum chow (CR group) for 12 weeks

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Summary

Introduction

Calorie restriction (CR), which has a potent anti-inflammaging effect, has been demonstrated to induce dramatic changes in the gut microbiota. Whether the modulated gut microbiota contributes to the attenuation of inflammation during CR is unknown, as are the members of the microbial community that may be key mediators of this process. Calorie restriction (CR) without malnutrition, which can extend lifespan and retard age-related diseases in many different organisms [1], has been demonstrated to modulate the gut microbiota and the profiles of microbial metabolites in serum or urine [2,3,4,5,6,7]. The gut microbiota, which can be directly modulated by CR, has been demonstrated to play a critical role in the pathogenesis and development of systemic inflammation. High-fat diet-induced dysbiosis of the gut microbiota damaged

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