scholarly journals Exploring the influence of the gut microbiota and probiotics on health: a symposium report

2014 ◽  
Vol 112 (S1) ◽  
pp. S1-S18 ◽  
Author(s):  
Linda V. Thomas ◽  
Theo Ockhuizen ◽  
Kaori Suzuki
Keyword(s):  
Gut Microbiota ◽  
Pathogenic Bacteria ◽  
Inflammatory Responses ◽  
Disease Risk ◽  
Ex Vivo ◽  
Inflammatory Diseases ◽  
Present Report ◽  
Keystone Species ◽  
Gut Barrier Function ◽  
The Impact

The present report describes the presentations delivered at the 7th International Yakult Symposium, ‘The Intestinal Microbiota and Probiotics: Exploiting Their Influence on Health’, in London on 22–23 April 2013. The following two themes associated with health risks were covered: (1) the impact of age and diet on the gut microbiota and (2) the gut microbiota's interaction with the host. The strong influence of the maternal gut microbiota on neonatal colonisation was reported, as well as rapid changes in the gut microbiome of older people who move from community living to residential care. The effects of dietary changes on gut metabolism were described and the potential influence of inter-individual microbiota differences was noted, in particular the presence/absence of keystone species involved in butyrate metabolism. Several speakers highlighted the association between certain metabolic disorders and imbalanced or less diverse microbiota. Data from metagenomic analyses and novel techniques (including anex vivohuman mucosa model) provided new insights into the microbiota's influence on coeliac, obesity-related and inflammatory diseases, as well as the potential of probiotics.Akkermansia muciniphilaandFaecalibacterium prausnitziiwere suggested as targets for intervention. Host–microbiota interactions were explored in the context of gut barrier function, pathogenic bacteria recognition, and the ability of the immune system to induce either tolerogenic or inflammatory responses. There was speculation that the gut microbiota should be considered a separate organ, and whether analysis of an individual's microbiota could be useful in identifying their disease risk and/or therapy; however, more research is needed into specific diseases, different population groups and microbial interventions including probiotics.

scholarly journals AMPK activates Parkin independent autophagy and improves post sepsis immune defense against secondary bacterial lung infections

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nathaniel B. Bone ◽  
Eugene J. Becker ◽  
Maroof Husain ◽  
Shaoning Jiang ◽  
Anna A. Zmijewska ◽  
...  
Keyword(s):  
Bacterial Infections ◽  
Pathogenic Bacteria ◽  
Inflammatory Responses ◽  
Abdominal Sepsis ◽  
Immune Defense ◽  
Bacterial Killing ◽  
Lung Infections ◽  
Sepsis Survivors ◽  
The Impact

AbstractMetabolic and bioenergetic plasticity of immune cells is essential for optimal responses to bacterial infections. AMPK and Parkin ubiquitin ligase are known to regulate mitochondrial quality control mitophagy that prevents unwanted inflammatory responses. However, it is not known if this evolutionarily conserved mechanism has been coopted by the host immune defense to eradicate bacterial pathogens and influence post-sepsis immunosuppression. Parkin, AMPK levels, and the effects of AMPK activators were investigated in human leukocytes from sepsis survivors as well as wild type and Park2−/− murine macrophages. In vivo, the impact of AMPK and Parkin was determined in mice subjected to polymicrobial intra-abdominal sepsis and secondary lung bacterial infections. Mice were treated with metformin during established immunosuppression. We showed that bacteria and mitochondria share mechanisms of autophagic killing/clearance triggered by sentinel events that involve depolarization of mitochondria and recruitment of Parkin in macrophages. Parkin-deficient mice/macrophages fail to form phagolysosomes and kill bacteria. This impairment of host defense is seen in the context of sepsis-induced immunosuppression with decreased levels of Parkin. AMPK activators, including metformin, stimulate Parkin-independent autophagy and bacterial killing in leukocytes from post-shock patients and in lungs of sepsis-immunosuppressed mice. Our results support a dual role of Parkin and AMPK in the clearance of dysfunctional mitochondria and killing of pathogenic bacteria, and explain the immunosuppressive phenotype associated Parkin and AMPK deficiency. AMPK activation appeared to be a crucial therapeutic target for the macrophage immunosuppressive phenotype and to reduce severity of secondary bacterial lung infections and respiratory failure.

scholarly journals One Health, Fermented Foods, and Gut Microbiota

Foods ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 195 ◽  
Author(s):  
Victoria Bell ◽  
Jorge Ferrão ◽  
Lígia Pimentel ◽  
Manuela Pintado ◽  
Tito Fernandes
Keyword(s):  
Lactic Acid ◽  
Gut Microbiota ◽  
One Health ◽  
Inflammatory Diseases ◽  
Animal Health ◽  
Saturated Fat ◽  
Well Being ◽  
Fermented Foods ◽  
Being There ◽  
The Impact

Changes in present-day society such as diets with more sugar, salt, and saturated fat, bad habits and unhealthy lifestyles contribute to the likelihood of the involvement of the microbiota in inflammatory diseases, which contribute to global epidemics of obesity, depression, and mental health concerns. The microbiota is presently one of the hottest areas of scientific and medical research, and exerts a marked influence on the host during homeostasis and disease. Fermented foods and beverages are generally defined as products made by microbial organisms and enzymatic conversions of major and minor food components. Further to the commonly-recognized effects of nutrition on the digestive health (e.g., dysbiosis) and well-being, there is now strong evidence for the impact of fermented foods and beverages (e.g., yoghurt, pickles, bread, kefir, beers, wines, mead), produced or preserved by the action of microorganisms, on general health, namely their significance on the gut microbiota balance and brain functionality. Fermented products require microorganisms, i.e., Saccharomyces yeasts and lactic acid bacteria, yielding alcohol and lactic acid. Ingestion of vibrant probiotics, especially those contained in fermented foods, is found to cause significant positive improvements in balancing intestinal permeability and barrier function. Our guts control and deal with every aspect of our health. How we digest our food and even the food sensitivities we have is linked with our mood, behavior, energy, weight, food cravings, hormone balance, immunity, and overall wellness. We highlight some impacts in this domain and debate calls for the convergence of interdisciplinary research fields from the United Nations’ initiative. Worldwide human and animal medicine are practiced separately; veterinary science and animal health are generally neither considered nor inserted within national or international Health discussions. The absence of a clear definition and subsequent vision for the future of One Health may act as a barrier to transdisciplinary collaboration. The point of this mini review is to highlight the role of fermented foods and beverages on gut microbiota and debate if the need for confluence of transdisciplinary fields of One Health is feasible and achievable, since they are managed by separate sectors with limited communication.

Piglets' gut microbiota dynamics.

2021 ◽  
Vol 16 (048) ◽  
Author(s):  
Daniela R. Klein
Keyword(s):  
Gut Microbiota ◽  
Pathogenic Bacteria ◽  
Cell Structure ◽  
Animal Health ◽  
Swine Production ◽  
Growth Promoters ◽  
Health Maintenance ◽  
Mortality And Morbidity ◽  
Weaning Piglets ◽  
The Impact

Abstract The gut microbiota has been a subject of great interest in recent years because the composition and diversity are associated with the maintenance of piglets' health and welfare. This review aims to summarise the composition and diversity of piglet microbiome, the impact on health maintenance, influence of feed and nutrients, impact of stress situations, and the effect of growth promoters and antimicrobials on gut microbiota. The composition and diversity of microbiota are influenced by animal early experiences, the appropriate development of microbiota is essential for intestinal function, and influence animal health, growth and productivity. Interactions between the gut microbiota and the immune system help maintain epithelial barrier, and protect from post-weaning diarrhoea pathogenies. After weaning, the piglets' diet changes abruptly, affecting the microbiota and the physiology, but this can be modulated through nutrients such as fibre, protein and minerals. Stress situations contribute to the appearance of intestinal disorders, possibly changing the microbiota and epithelial cell structure, facilitating colonisation of pathogenic bacteria, decreased performance and increase the use of antimicrobials. In swine production, growth promoters and antibiotics are used to reduce mortality and morbidity, especially in weaning piglets, reducing and controlling potential pathogenic bacteria, resulting in more feed intake and body weight. Antimicrobial use reduces the entire gut microbial population; the replacers are probiotics, prebiotics and organic acids, which helps maintain intestinal microbial populations, and inhibits pathogenic bacteria development. Knowing the animal microbiome dynamics helps improve immunity, productive performance and welfare, and also reduce the use of antimicrobials in animal production.

scholarly journals Intestinal IgA Regulates Expression of a Fructan Polysaccharide Utilization Locus in Colonizing Gut Commensal Bacteroides thetaiotaomicron

mBio ◽  
2019 ◽  
Vol 10 (6) ◽  
Author(s):  
Payal Joglekar ◽  
Hua Ding ◽  
Pablo Canales-Herrerias ◽  
Pankaj Jay Pasricha ◽  
Justin L. Sonnenburg ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Ex Vivo ◽  
Microbial Colonization ◽  
Bacteroides Thetaiotaomicron ◽  
Content Type ◽  
Microbial Utilization ◽  
Polysaccharide Utilization Locus ◽  
The Impact

ABSTRACT Gut-derived immunoglobulin A (IgA) is the most abundant antibody secreted in the gut that shapes gut microbiota composition and functionality. However, most of the microbial antigens targeted by gut IgA remain unknown, and the functional effects of IgA targeting these antigens are currently understudied. This study provides a framework for identifying and characterizing gut microbiota antigens targeted by gut IgA. We developed a small intestinal ex vivo culture assay to harvest lamina propria IgA from gnotobiotic mice, with the aim of identifying antigenic targets in a model human gut commensal, Bacteroides thetaiotaomicron VPI-5482. Colonization by B. thetaiotaomicron induced a microbe-specific IgA response that was reactive against diverse antigens, including capsular polysaccharides, lipopolysaccharides, and proteins. IgA against microbial protein antigens targeted membrane and secreted proteins with diverse functionalities, including an IgA specific against proteins of the polysaccharide utilization locus (PUL) that are necessary for utilization of fructan, which is an important dietary polysaccharide. Further analyses demonstrated that the presence of dietary fructan increased the production of fructan PUL-specific IgA, which then downregulated the expression of fructan PUL in B. thetaiotaomicron, both in vivo and in vitro. Since the expression of fructan PUL has been associated with the ability of B. thetaiotaomicron to colonize the gut in the presence of dietary fructans, our work suggests a novel role for gut IgA in regulating microbial colonization by modulating their metabolism. IMPORTANCE Given the significant impact that gut microbes have on our health, it is essential to identify key host and environmental factors that shape this diverse community. While many studies have highlighted the impact of diet on gut microbiota, little is known about how the host regulates this critical diet-microbiota interaction. In our present study, we discovered that gut IgA targeted a protein complex involved in the utilization of an important dietary polysaccharide: fructan. While the presence of dietary fructans was previously thought to allow unrestricted growth of fructan-utilizing bacteria, our work shows that gut IgA, by targeting proteins responsible for fructan utilization, provides the host with tools that can restrict the microbial utilization of such polysaccharides, thereby controlling their growth.

Advanced glycation end products (AGEs) in metabolic disease: linking diet, inflammation and microbiota

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Giulia Gaudioso ◽  
Debora Collotta ◽  
Fausto Chiazza ◽  
Raffaella Mastrocola ◽  
Alessia Cento ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Gut Microbiota ◽  
Advanced Glycation End Products ◽  
Disease Risk ◽  
In Vivo Studies ◽  
Blood Levels ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
The Impact

AbstractIntroduction:High sugar consumption promotes endogenous formation of advanced glycation end-products (AGEs), a heterogeneous class of molecules originated from non-enzymatic glycation between reducing sugars and free amino groups of proteins, nucleic acids, or lipids. AGEs accumulation in tissues has been linked to aging and diabetes complications. AGEs might also play an independent role in inflammation and development of cardiovascular disease (CVD). Exogenous dietary AGEs, due to excess intake of modern heat-treated foods, might act synergistically with endogenous AGEs, thus contributing to increase inflammation and CVD. A large amount of ingested AGEs reaches the colon, where they might affect gut microbial metabolism, for example, by acting as substrate for colonic bacterial fermentation, driving alterations of microbiota composition and of intestinal permeability. However in vitro and in vivo studies (animal and human) on the impact of AGEs on the gut microbiota are discordant. This study on mice aims to link the modulation of gut microbiota by AGEs-enriched diet (AGE-D) with metabolic and inflammatory markers.Materials and methods:C57BL/6 mice were randomly allocated into the following dietary regimens: Control (n = 24) and AGE-D (n = 20) for 22 weeks. AGE-D was prepared replacing casein (200 g/kg diet) by an equal amount of modified casein where 10% of arginine was glycated with MG-H1 (methylglyoxal 5-hydro-5-methylimidazolone) for a total of 4 μmol of MG-H1 per g of diet. Faeces were collected using metabolic cages (18 h starving) at week 0, 11 and 22 for fecal DNA extraction and 16SrRNA analysis through Illumina MiSeq using V3-V4 targeted primers. After 22 weeks of dietary manipulation, mice were sacrificed, plasma and organ lipid profiles and serum metabolic and inflammatory profiles were determined.Results and discussion:AGE-D caused a significant reduction in the blood levels of two important components of the incretin system, GIP and GLP-1, when compared to control diet, suggestive of unbalance in the incretin-insulin axis. AGE-D exposure was associated with a significant increase in systemic concentrations of inflammatory cytokines, e.g. IL-1β and IL-17, and PAI-1, which has been suggested as both reliable marker and critical mediator of cellular senescence. We will present how AGEs impact on microbiome community structure and correlate changes in gut microbiota with GIP and GLP-1 levels.Conclusions:AGEs, characteristic of modern processed foods, appear to impact on the incretin-insulin axis, a key regulator of metabolic disease risk. Diets rich in AGEs may mediate these physiological effects at least in part, by reshaping intestinal microbiota structure.

scholarly journals Increased soluble amyloid-beta causes early aberrant brain network hypersynchronisation in a mature-onset mouse model of amyloidosis

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Inès R. H. Ben-Nejma ◽  
Aneta J. Keliris ◽  
Jasmijn Daans ◽  
Peter Ponsaerts ◽  
Marleen Verhoye ◽  
...  
Keyword(s):  
Mouse Model ◽  
Postnatal Development ◽  
Amyloid Beta ◽  
Resting State ◽  
Inflammatory Responses ◽  
Ex Vivo ◽  
Fold Increase ◽  
Brain Network ◽  
Resting State Networks ◽  
The Impact

AbstractAlzheimer’s disease (AD) is the most common form of dementia in the elderly. According to the amyloid hypothesis, the accumulation and deposition of amyloid-beta (Aβ) peptides play a key role in AD. Soluble Aβ (sAβ) oligomers were shown to be involved in pathological hypersynchronisation of brain resting-state networks in different transgenic developmental-onset mouse models of amyloidosis. However, the impact of protein overexpression during brain postnatal development may cause additional phenotypes unrelated to AD. To address this concern, we investigated sAβ effects on functional resting-state networks in transgenic mature-onset amyloidosis Tet-Off APP (TG) mice. TG mice and control littermates were raised on doxycycline (DOX) diet from 3d up to 3 m of age to suppress transgenic Aβ production. Thereafter, longitudinal resting-state functional MRI was performed on a 9.4 T MR-system starting from week 0 (3 m old mice) up to 28w post DOX treatment. Ex-vivo immunohistochemistry and ELISA analysis was performed to assess the development of amyloid pathology. Functional Connectivity (FC) analysis demonstrated early abnormal hypersynchronisation in the TG mice compared to the controls at 8w post DOX treatment, particularly across regions of the default mode-like network, known to be affected in AD. Ex-vivo analyses performed at this time point confirmed a 20-fold increase in total sAβ levels preceding the apparition of Aβ plaques and inflammatory responses in the TG mice compared to the controls. On the contrary at week 28, TG mice showed an overall hypoconnectivity, coinciding with a widespread deposition of Aβ plaques in the brain. By preventing developmental influence of APP and/or sAβ during brain postnatal development, we demonstrated FC abnormalities potentially driven by sAβ neurotoxicity on resting-state neuronal networks in mature-induced TG mice. Thus, the Tet-Off APP mouse model could be a powerful tool while used as a mature-onset model to shed light into amyloidosis mechanisms in AD.

Aspirin and P2Y12 Inhibitors in platelet-mediated activation of neutrophils and monocytes

2015 ◽  
Vol 114 (09) ◽  
pp. 478-789 ◽  
Author(s):  
Waltraud Schrottmaier ◽  
Julia Kral ◽  
Sigrun Badrnya ◽  
Alice Assinger
Keyword(s):  
Immune Responses ◽  
Antiplatelet Therapy ◽  
Inflammatory Responses ◽  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Cardiovascular Complications ◽  
P2y12 Inhibitors ◽  
Beneficial Effects ◽  
Cox Inhibitor ◽  
The Impact

SummaryPlatelets are key players in haemostasis and represent a pivotal link between inflammation, immunity and atherogenesis. Depending on the (patho)physiological environment platelets modulate various leukocyte functions via release of inflammatory mediators and direct cell-cell interactions. Elevated levels of circulating platelet-leukocyte aggregates are found in patients suffering from several thrombotic or inflammatory conditions. Platelet-monocyte and platelet-neutrophil interaction can trigger pro- and anti-inflammatory responses and modulate effector functions of all leukocyte subpopulations. These platelet-mediated immune responses have implications for the progression of cardiovascular diseases and also play a crucial role during infections, cancer, transplantations and other inflammatory diseases of several organs. Antiplatelet therapy including the COX inhibitor aspirin and/or ADP receptor P2Y12 inhibitors such as clopidogrel, prasugrel and ticagrelor are the therapy of choice for various cardiovascular complications. Both aspirin and P2Y12 inhibitors attenuate platelet-leukocyte interactions, thereby also modulating immune responses. This may have beneficial effects in some pathological conditions, while it might be detrimental in others. This review aims to summarise the current knowledge on platelet-leukocyte interactions and the impact of aspirin and P2Y12 inhibition on platelet-mediated immune responses and to give an overview on the effects of antiplatelet therapy on platelet-leukocyte interplay in various diseases.

scholarly journals Regulation of common neurological disorders by gut microbial metabolites

2021 ◽  
Author(s):  
Jeongho Park ◽  
Chang H. Kim
Keyword(s):  
Neurological Disorders ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Short Chain Fatty Acids ◽  
Autism Spectrum ◽  
Molecular Networks ◽  
Microbial Metabolites ◽  
Cns Diseases ◽  
The Impact

AbstractThe gut is connected to the CNS by immunological mediators, lymphocytes, neurotransmitters, microbes and microbial metabolites. A mounting body of evidence indicates that the microbiome exerts significant effects on immune cells and CNS cells. These effects frequently result in the suppression or exacerbation of inflammatory responses, the latter of which can lead to severe tissue damage, altered synapse formation and disrupted maintenance of the CNS. Herein, we review recent progress in research on the microbial regulation of CNS diseases with a focus on major gut microbial metabolites, such as short-chain fatty acids, tryptophan metabolites, and secondary bile acids. Pathological changes in the CNS are associated with dysbiosis and altered levels of microbial metabolites, which can further exacerbate various neurological disorders. The cellular and molecular mechanisms by which these gut microbial metabolites regulate inflammatory diseases in the CNS are discussed. We highlight the similarities and differences in the impact on four major CNS diseases, i.e., multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, and autism spectrum disorder, to identify common cellular and molecular networks governing the regulation of cellular constituents and pathogenesis in the CNS by microbial metabolites.

scholarly journals Dooming Phagocyte Responses: Inflammatory Effects of Endogenous Oxidized Phospholipids

2021 ◽  
Vol 12 ◽  
Author(s):  
Marco Di Gioia ◽  
Ivan Zanoni
Keyword(s):  
Immune Cells ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Biological Activities ◽  
Oxidized Lipids ◽  
Oxidized Phospholipids ◽  
Clinical Tools ◽  
Stress Mediators ◽  
The Impact

Endogenous oxidized phospholipids are produced during tissue stress and are responsible for sustaining inflammatory responses in immune as well as non-immune cells. Their local and systemic production and accumulation is associated with the etiology and progression of several inflammatory diseases, but the molecular mechanisms that underlie the biological activities of these oxidized phospholipids remain elusive. Increasing evidence highlights the ability of these stress mediators to modulate cellular metabolism and pro-inflammatory signaling in phagocytes, such as macrophages and dendritic cells, and to alter the activation and polarization of these cells. Because these immune cells serve a key role in maintaining tissue homeostasis and organ function, understanding how endogenous oxidized lipids reshape phagocyte biology and function is vital for designing clinical tools and interventions for preventing, slowing down, or resolving chronic inflammatory disorders that are driven by phagocyte dysfunction. Here, we discuss the metabolic and signaling processes elicited by endogenous oxidized lipids and outline new hypotheses and models to elucidate the impact of these lipids on phagocytes and inflammation.

scholarly journals A Novel View of Human Helicobacter pylori Infections: Interplay between Microbiota and Beta-Defensins

Biomolecules ◽  
2019 ◽  
Vol 9 (6) ◽  
pp. 237 ◽  
Author(s):  
Pero ◽  
Brancaccio ◽  
Laneri ◽  
Biasi ◽  
Lombardo ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Immune System ◽  
Gut Microbiota ◽  
Host Response ◽  
Pathogenic Bacteria ◽  
Precancerous Lesions ◽  
Innate Immune ◽  
Microbial Infections ◽  
Beta Defensins ◽  
The Impact

The gut microbiota is significantly involved in the preservation of the immune system of the host, protecting it against the pathogenic bacteria of the stomach. The correlation between gut microbiota and the host response supports human gastric homeostasis. Gut microbes may be shifted in Helicobacter pylori (Hp)-infected individuals to advance gastric inflammation and distinguished diseases. Particularly interesting is the establishment of cooperation between gut microbiota and antimicrobial peptides (AMPs) of the host in the gastrointestinal tract. AMPs have great importance in the innate immune reactions to Hp and participate in conservative co-evolution with an intricate microbiome. β-Defensins, a class of short, cationic, arginine-rich proteins belonging to the AMP group, are produced by epithelial and immunological cells. Their expression is enhanced during Hp infection. In this review, we discuss the impact of the gut microbiome on the host response, with particular regard to β-defensins in Hp-associated infections. In microbial infections, mostly in precancerous lesions induced by Hp infection, these modifications could lead to different outcomes.

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