Reciprocal interactions between gut microbiota and autophagy

Abstract

A symbiotic relationship has set up between the gut microbiota and its host in the course of evolution, forming an interkingdom consortium. The gut offers a favorable ecological niche for microbial communities, with the whole body and external factors ( e.g. , diet or medications) contributing to modulating this microenvironment. Reciprocally, the gut microbiota is important for maintaining health by acting not only on the gut mucosa but also on other organs. However, failure in one or another of these two partners can lead to the breakdown in their symbiotic equilibrium and contribute to disease onset and/or progression. Several microbial and host processes are devoted to facing up the stress that could alter the symbiosis, ensuring the resilience of the ecosystem. Among these processes, autophagy is a host catabolic process integrating a wide range of stress in order to maintain cell survival and homeostasis. This cytoprotective mechanism, which is ubiquitous and operates at basal level in all tissues, can be rapidly down- or up-regulated at the transcriptional, post-transcriptional, or post-translational levels, to respond to various stress conditions. Because of its sensitivity to all, metabolic-, immune-, and microbial-derived stimuli, autophagy is at the crossroad of the dialogue between changes occurring in the gut microbiota and the host responses. In this review, we first delineate the modulation of host autophagy by the gut microbiota locally in the gut and in peripheral organs. Then, we describe the autophagy-related mechanisms affecting the gut microbiota. We conclude this review with the current challenges and an outlook toward the future interventions aiming at modulating host autophagy by targeting the gut microbiota.

Metabolic Role of Autophagy in the Pathogenesis and Development of NAFLD

“…Emerging evidence supports that the gut microbiota may contribute to liver diseases through multiple mechanisms influenced by bacterial composition [ 91 ]. The reciprocal interactions between the gut microbiota and autophagy have been well described in previous reviews [ 92 , 93 ]. In general, autophagy deficiency leads to an altered composition and diversity of the gut microbiota, resulting in dysbiosis.…”

Regulation of autophagy by plant‐based polyphenols: A critical review of current advances in glucolipid metabolic diseases and food industry applications

“…Fusobacterium nucleatum) and gut metabolites (e.g., lipopolysaccharide, secondary biliary acids, cytokines, hormones) can modulate autophagy and thus stimulate extensive host molecular sensors (Lapaquette et al, 2021). Currently, whether polyphenols can modulate autophagy by modifying gut microbiota and microbiota-derived products to improve GLMDs has not been reported and therefore deserves further investigation.…”

“…These findings reveal that polyphenols maintain intestinal homeostasis and relieve intestinal inflammation by activating autophagy. Nevertheless, it is important to note that some intestinal microflora (e.g., Lacticaseibacillus , Lactobacillus , Bifidobacterium , Butyrivibrio fibrisolvens , Megamonas , Roseburia , Desulfovibrio , Ruminococcus genus, and Fusobacterium nucleatum ) and gut metabolites (e.g., lipopolysaccharide, secondary biliary acids, cytokines, hormones) can modulate autophagy and thus stimulate extensive host molecular sensors (Lapaquette et al., 2021). Currently, whether polyphenols can modulate autophagy by modifying gut microbiota and microbiota‐derived products to improve GLMDs has not been reported and therefore deserves further investigation.…”

Gut Microbiota in Autophagy Regulation: New Therapeutic Perspective in Neurodegeneration

“…Numerous in vivo studies suggested that gut microbiota-derived metabolites, including neurotransmitters, neuromodulator peptides, short-chain fatty acids (SCFAs), and LPSs, influence attenuating neuroinflammation [21,22]. Studies have reported that gut metabolites are vital in regulating neurodegenerative and neuroinflammatory disorders [5,23,24] by initiating autophagy [25,26].…”