Long-term intake of Lactobacillus helveticus enhances bioavailability of omega-3 fatty acids in the mouse retina.

Omega-3 (n-3) polyunsaturated fatty acids (PUFAs), particularly docosahexaenoic acid (DHA), are required for the structure and function of the retina. Several observational studies indicate that consumption of a diet with relatively high levels of n-3 PUFAs, such as those provided by fish oils, has a protective effect against the development of age-related macular degeneration. Given the accumulating evidence showing the role of gut microbiota in regulating retinal physiology and host lipid metabolism, we evaluated the potential of long-term dietary supplementation with the Gram-positive bacterium Lactobacillus helveticus strain VEL12193 to modulate the retinal n-3 PUFA content.

Spontaneous Prophage Induction Contributes to the Production of Membrane Vesicles by the Gram-Positive Bacterium BL23.

The formation of membrane vesicles (MVs) by Gram-positive bacteria has gained increasing attention over the last decade. Recently, models of vesicle formation have been proposed and involve the digestion of the cell wall by prophage-encoded or stress-induced peptidoglycan (PG) hydrolases and the inhibition of PG synthesis by β-lactam antibiotics. The impact of these mechanisms on vesicle formation is largely dependent on the strain and growth conditions.

You shall not pass! Protective role of autophagic machinery in response to plasma membrane damage triggered by invasion.

Candida albicans (C. albicans) is an opportunistic pathogen causing infections ranging from superficial to life-threatening dissemination, in which C. albicans is able to translocate through the gut barrier into deeper organs.

Membrane protective role of autophagic machinery during infection of epithelial cells by .

() is an opportunistic pathogen causing infections ranging from superficial to life-threatening disseminated infections. In a susceptible host, is able to translocate through the gut barrier, promoting its dissemination into deeper organs. hyphae can invade human epithelial cells by two well-documented mechanisms: epithelial-driven endocytosis and -driven active penetration.

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 (, 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.

Intestinal release of biofilm-like microcolonies encased in calcium-pectinate beads increases probiotic properties of Lacticaseibacillus paracasei.

In this study, we show that calcium pectinate beads (CPB) allow the formation of 20 µm spherical microcolonies of the probiotic bacteria Lacticaseibacillus paracasei (formerly designated as Lactobacillus paracasei) ATCC334 with a high cell density, reaching more than 10 log (CFU/g). The bacteria within these microcolonies are well structured and adhere to a three-dimensional network made of calcium-pectinate through the synthesis of extracellular polymeric substances (EPS) and thus display a biofilm-like phenotype, an attractive property for their use as probiotics. During bacterial development in the CPB, a coalescence phenomenon arises between neighboring microcolonies accompanied by their peripheral spatialization within the bead.

Resveratrol Favors Adhesion and Biofilm Formation of Strain ATCC334.

Bacterial strains of the Lactobacillaceae family are widely used as probiotics for their multifaceted potential beneficial properties. However, no official recommendations for their clinical use exist since, in many cases, oral administrations of these bacteria displayed limited beneficial effects in human. Additional research is thus needed to improve the efficiency of existing strains with strong potential.

" Interactions With The Host: Crossing The Intestinal Epithelial Barrier".

Formerly a commensal organism of the mucosal surfaces of most healthy individuals, is an opportunistic pathogen that causes infections ranging from superficial to the more life-threatening disseminated infections, especially in the ever-growing population of vulnerable patients in the hospital setting. In these situations, the fungus takes advantage of its host following a disturbance in the host defense system and/or the mucosal microbiota. Overwhelming evidence suggests that the gastrointestinal tract is the main source of disseminated infections.

Resveratrol-Induced Xenophagy Promotes Intracellular Bacteria Clearance in Intestinal Epithelial Cells and Macrophages.

Autophagy is a lysosomal degradation process that contributes to host immunity by eliminating invasive pathogens and the modulating inflammatory response. Several infectious and immune disorders are associated with autophagy defects, suggesting that stimulation of autophagy in these diseases should be beneficial. Here, we show that resveratrol is able to boost xenophagy, a selective form of autophagy that target invasive bacteria.

entry unveils a calcium/calpain-dependent mechanism for inhibiting sumoylation.

Disruption of the sumoylation/desumoylation equilibrium is associated with several disease states such as cancer and infections, however the mechanisms regulating the global SUMO balance remain poorly defined. Here, we show that infection by , the causative agent of human bacillary dysentery, switches off host sumoylation during epithelial cell infection in vitro and in vivo and that this effect is mainly mediated by a calcium/calpain-induced cleavage of the SUMO E1 enzyme SAE2, thus leading to sumoylation inhibition. Furthermore, we describe a mechanism by which promotes its own invasion by altering the sumoylation state of RhoGDIα, a master negative regulator of RhoGTPase activity and actin polymerization.

[Regulation of immunity and inflammation by autophagy: « All is well, all is fine, all goes as well as possible»].

Autophagy is a lysosomal degradation mechanism which helps to control intracellular infections and contributes to the regulation of innate and adaptive immune responses. Defects in autophagy lead to exacerbated proliferation of microorganisms and/or to excessive immune responses which are both highly deleterious. Thus, infectious and chronic inflammatory human diseases, such as Crohn's disease, are often associated with inappropriate modulation of autophagy, which is mainly linked to autophagy-associated gene polymorphisms.

Sumoylation coordinates the repression of inflammatory and anti-viral gene-expression programs during innate sensing.

Innate sensing of pathogens initiates inflammatory cytokine responses that need to be tightly controlled. We found here that after engagement of Toll-like receptors (TLRs) in myeloid cells, deficient sumoylation caused increased secretion of transcription factor NF-κB-dependent inflammatory cytokines and a massive type I interferon signature. In mice, diminished sumoylation conferred susceptibility to endotoxin shock and resistance to viral infection.

Cellular and Molecular Connections between Autophagy and Inflammation.

Autophagy is an intracellular catabolic pathway essential for the recycling of proteins and larger substrates such as aggregates, apoptotic corpses, or long-lived and superfluous organelles whose accumulation could be toxic for cells. Because of its unique feature to engulf part of cytoplasm in double-membrane cup-shaped structures, which further fuses with lysosomes, autophagy is also involved in the elimination of host cell invaders and takes an active part of the innate and adaptive immune response. Its pivotal role in maintenance of the inflammatory balance makes dysfunctions of the autophagy process having important pathological consequences.

Sumoylation of human argonaute 2 at lysine-402 regulates its stability.

Gene silencing by small RNAs has emerged as a powerful post-transcriptional regulator of gene expression, however processes underlying regulation of the small RNA pathway in vivo are still largely elusive. Here, we identified sumoylation as a novel post-translational modification acting on Ago2, the main effector of small RNA-mediated gene silencing. We demonstrate that Ago2 can be modified by SUMO1 and SUMO2/3 and identified Lys402 as the major Ago2 sumoylation site in vivo.

Sumoylation at chromatin governs coordinated repression of a transcriptional program essential for cell growth and proliferation.

Despite numerous studies on specific sumoylated transcriptional regulators, the global role of SUMO on chromatin in relation to transcription regulation remains largely unknown. Here, we determined the genome-wide localization of SUMO1 and SUMO2/3, as well as of UBC9 (encoded by UBE2I) and PIASY (encoded by PIAS4), two markers for active sumoylation, along with Pol II and histone marks in proliferating versus senescent human fibroblasts together with gene expression profiling. We found that, whereas SUMO alone is widely distributed over the genome with strong association at active promoters, active sumoylation occurs most prominently at promoters of histone and protein biogenesis genes, as well as Pol I rRNAs and Pol III tRNAs.

Autophagy and Crohn's disease.

Advances in genetics have shed light on the molecular basis of Crohn's disease (CD) predisposition and pathogenesis, via linkage disequilibrium analysis to genome-wide association studies. The discovery of genetic variants of NOD2, an intracellular pathogen molecular sensor, as risk factors for CD has paved the way for further research on innate immunity in this disease. Remarkably, polymorphisms in autophagy genes, such as ATG16L1 and IRGM, have been identified, allowing the pivotal role of autophagy in innate immunity to be uncovered.

Guidelines for the use and interpretation of assays for monitoring autophagy.

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding.

Etiology of Crohn's disease: many roads lead to autophagy.

Crohn's disease is a complex multifactor diseases that occur in individuals with genetic predisposition in whom environmental and microbial triggers cause a deleterious chronic immune response. Susceptibility to Crohn's disease is influenced by common variants at many loci. Genetic studies have emphasized the role of host susceptibility in inflammatory bowel disease onset with the identification of about 100 risk loci, most of which encode proteins involved in immunity, host defense against microbes, and gut homeostasis.

Defects in autophagy favour adherent-invasive Escherichia coli persistence within macrophages leading to increased pro-inflammatory response.

Ileal lesions in Crohn's disease (CD) patients are abnormally colonized by pathogenic adherent-invasive Escherichia coli (AIEC). AIEC bacteria are able to replicate within epithelial cells after lysis of the endocytic vacuole and within macrophages in a large vacuole. CD-associated polymorphisms in NOD2, ATG16L1 and IRGM affect bacterial autophagy, a crucial innate immunity mechanism.

Risk predisposition for Crohn disease: a "ménage à trois" combining IRGM allele, miRNA and xenophagy.

Susceptibility to Crohn disease (CD), an inflammatory bowel disease, is influenced by common variants at many loci like the exonic synonymous IRGM SNP (rs10065172, NM_001145805.1, c.313C>T).