Reciprocal interactions between gut microbiota and autophagy

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 upregulated 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.

Autism and carnitine: A possible link

Patients with autism spectrum disorders(ASD) present deficits in social interactions and communication, they also show limited and stereotypical patterns of behaviors and interests. The pathophysiological bases of ASD have not been defined yet. Many factors seem to be involved in the onset of this disorder. These include genetic and environmental factors, but autism is not linked to a single origin, only. Autism onset can be connected with various factors such as metabolic disorders: including carnitine deficiency. Carnitine is a derivative of two amino acid lysine and methionine. Carnitine is a cofactor for a large family of enzymes: the carnitine acyltransferases. Through their action these enzymes(and L-carnitine) are involved in energy production and metabolic homeostasis. Some people with autism(less than 20%) seem to have L-carnitine metabolism disorders and for these patients, a dietary supplementation with Lcarnitine is beneficial. This review summarizes the available information on this topic.

Interaction of Escherichia coli heat-labile enterotoxin B-pentamer with exopolysaccharides from Leuconostoc mesenteroides P35:Insights from surface plasmon resonance and molecular docking studies

In this study,the interaction of exopolysaccharides from Leuconostoc mesenteroides P35(EPS-LM)with Escherichia coli heat-labile enterotoxin B-pentamer(LTB)was investigated at different concentrations and temperatures by using surface plasmon resonance(SPR)and molecular docking approaches.FT-IR spectral analysis together with HPTLC analysis revealing that glucose is the only constitutive monosaccharide of EPS-LM suggests that its structure is composed of dextran withα-D(1→6)glycosidic linkages.SPR analysis revealed the high affinity of EPS-LM for immobilized LTB toxin(KA=(2.05±0.04)×106 mol.L−1 at 37°C).The binding process was spontaneous(ΔG<0),endothermic(ΔH>0),and entropy-driven(ΔS>0)with an increase of KA with temperature.This suggests that EPS-LM-LTB interaction is dominated by hydrophobic forces.The binding affinity of EPS-LM to LTB had negligible dependence on enthalpy(ΔH=0.084 kJ mol−1).Further,molecular docking results suggested the presence of some binding sites of EPS-LM on the LTB through hydrophobic forces(Lys,Asp,Arg,Glu)and also hydrogen bonding(Glu)in the hydrophobic core of LTB.Besides autodock studies,Schiffer-Edmundson helical wheel diagrams of LTB inα-helix domain suggested that LTB hydrophobic core is a highly effective region,which was able to form favorable non-polar interactions of the protein's binding surface(with amino acids residues such as Tyr,Leu,Ile)with EPS-LM.This study provided thus further insights into the interactions between EPS-LM and LTB,suggesting that EPS produced by some LAB,such as EPS produced by Ln.mesenteroides P35 strain are good candidates to inhibit E.coli toxin activity.