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The potential of probiotics in the amelioration of hyperuricemia.
Zhao, H, Lu, Z, Lu, Y
Food & function. 2022;(5):2394-2414
Abstract
Hyperuricemia is a common disease caused by metabolic disorders or the excessive intake of high-purine foods. Persistent hyperuricemia in extreme cases induces gout, and asymptomatic hyperuricemia is probably linked to other metabolic diseases, such as hypertension. The typical damage caused by asymptomatic hyperuricemia includes inflammation, oxidative stress and gut dysbiosis. Probiotics have broad potential applications as food additives, not as drug therapies, in the amelioration of hyperuricemia. In this review, we describe novel methods for potential hyperuricemia amelioration with probiotics. The pathways through which probiotics may ameliorate hyperuricemia are discussed, including the decrease in uric acid production through purine assimilation and XOD (xanthine oxidase) inhibition as well as enhanced excretion of uric acid production by promoting ABCG2 (ATP binding cassette subfamily G member 2) activity, respectively. Three possible probiotic-related therapeutic pathways for alleviating the syndrome of hyperuricemia are also summarized. The first mechanism is to alleviate the oxidation and inflammation induced by hyperuricemia through the inhibition of NLRP3 inflammasome, the second is to restore damaged intestinal epithelium barriers and prevent gut microbiota dysbiosis, and the third is to enhance the innate immune system by increasing the secretion of immunoglobulin A (sIgA) to resist the stimulus by hyperuricemia. We propose that future research should focus on superior strain resource isolation and insight into the cause-effect mechanisms of probiotics for hyperuricemia amelioration. The safety and effects of the application of probiotics in clinical use also need verification.
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Sepsis-Induced Myopathy and Gut Microbiome Dysbiosis: Mechanistic Links and Therapeutic Targets.
Mankowski, RT, Laitano, O, Darden, D, Kelly, L, Munley, J, Loftus, TJ, Mohr, AM, Efron, PA, Thomas, RM
Shock (Augusta, Ga.). 2022;(1):15-23
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Abstract
Sepsis is currently defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. The skeletal muscle system is among the host organ systems compromised by sepsis. The resulting neuromuscular dysfunction and impaired regenerative capacity defines sepsis-induced myopathy and manifests as atrophy, loss of strength, and hindered regeneration after injury. These outcomes delay recovery from critical illness and confer increased vulnerability to morbidity and mortality. The mechanisms underlying sepsis-induced myopathy, including the potential contribution of peripheral organs, remain largely unexplored. The gut microbiome is an immunological and homeostatic entity that interacts with and controls end-organ function, including the skeletal muscle system. Sepsis induces alterations in the gut microbiota composition, which is globally termed a state of "dysbiosis" for the host compared to baseline microbiota composition. In this review, we critically evaluate existing evidence and potential mechanisms linking sepsis-induced myopathy with gut microbiota dysbiosis.
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The gut microbiota in retinal diseases.
Bringer, MA, Gabrielle, PH, Bron, AM, Creuzot-Garcher, C, Acar, N
Experimental eye research. 2022;:108867
Abstract
The gut microbiota is a complex ecosystem that inhabits the gastrointestinal tract and consists of archaea, fungi, viruses, and bacteria, with bacteria being dominant. From birth onwards, it coevolves dynamically together with the host. The composition of the gut microbiota is under the influence of a complex interplay between both host and environmental factors. Scientific advances in the past few decades have shown that it is essential in maintaining homeostasis and tipping the balance between health and disease. In addition to its role in food digestion, the gut microbiota is implicated in regulating multiple physiological processes in the host gut mucosa and in distant organs such as the brain. Persistent imbalance between gut microbial communities, termed "dysbiosis," has been associated with several inflammatory and metabolic diseases as well as with central nervous system disorders. In this review, we present the state of the art of current knowledge on an emerging concept, the microbiota-retina axis, and the potential role of its disturbance in the development of retinopathies. We also describe several microbiota-targeting strategies that could constitute preventive and therapeutic tools for retinopathies.
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European guideline on indications, performance, and clinical impact of hydrogen and methane breath tests in adult and pediatric patients: European Association for Gastroenterology, Endoscopy and Nutrition, European Society of Neurogastroenterology and Motility, and European Society for Paediatric Gastroenterology Hepatology and Nutrition consensus.
Hammer, HF, Fox, MR, Keller, J, Salvatore, S, Basilisco, G, Hammer, J, Lopetuso, L, Benninga, M, Borrelli, O, Dumitrascu, D, et al
United European gastroenterology journal. 2022;(1):15-40
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Abstract
INTRODUCTION Measurement of breath hydrogen (H2 ) and methane (CH4 ) excretion after ingestion of test-carbohydrates is used for different diagnostic purposes. There is a lack of standardization among centers performing these tests and this, together with recent technical developments and evidence from clinical studies, highlight the need for a European guideline. METHODS This consensus-based clinical practice guideline defines the clinical indications, performance, and interpretation of H2 -CH4 -breath tests in adult and pediatric patients. A balance between scientific evidence and clinical experience was achieved by a Delphi consensus that involved 44 experts from 18 European countries. Eighty eight statements and recommendations were drafted based on a review of the literature. Consensus (≥80% agreement) was reached for 82. Quality of evidence was evaluated using validated criteria. RESULTS The guideline incorporates new insights into the role of symptom assessment to diagnose carbohydrate (e.g., lactose) intolerances and recommends that breath tests for carbohydrate malabsorption require additional validated concurrent symptom evaluation to establish carbohydrate intolerance. Regarding the use of breath tests for the evaluation of oro-cecal transit time and suspected small bowel bacterial overgrowth, this guideline highlights confounding factors associated with the interpretation of H2 -CH4 -breath tests in these indications and recommends approaches to mitigate these issues. CONCLUSION This clinical practice guideline should facilitate pan-European harmonization of diagnostic approaches to symptoms and disorders, which are very common in specialist and primary care gastroenterology practice, both in adult and pediatric patients. In addition, it identifies areas of future research needs to clarify diagnostic and therapeutic approaches.
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Infants with cystic fibrosis have altered fecal functional capacities with potential clinical and metabolic consequences.
Eng, A, Hayden, HS, Pope, CE, Brittnacher, MJ, Vo, AT, Weiss, EJ, Hager, KR, Leung, DH, Heltshe, SL, Raftery, D, et al
BMC microbiology. 2021;(1):247
Abstract
BACKGROUND Infants with cystic fibrosis (CF) suffer from gastrointestinal (GI) complications, including pancreatic insufficiency and intestinal inflammation, which have been associated with impaired nutrition and growth. Recent evidence identified altered fecal microbiota taxonomic compositions in infants with CF relative to healthy infants that were characterized by differences in the abundances of taxa associated with GI health and nutrition. Furthermore, these taxonomic differences were more pronounced in low length infants with CF, suggesting a potential link to linear growth failure. We hypothesized that these differences would entail shifts in the microbiome's functional capacities that could contribute to inflammation and nutritional failure in infants with CF. RESULTS To test this hypothesis, we compared fecal microbial metagenomic content between healthy infants and infants with CF, supplemented with an analysis of fecal metabolomes in infants with CF. We identified notable differences in CF fecal microbial functional capacities, including metabolic and environmental response functions, compared to healthy infants that intensified during the first year of life. A machine learning-based longitudinal metagenomic age analysis of healthy and CF fecal metagenomic functional profiles further demonstrated that these differences are characterized by a CF-associated delay in the development of these functional capacities. Moreover, we found metagenomic differences in functions related to metabolism among infants with CF that were associated with diet and antibiotic exposure, and identified several taxa as potential drivers of these functional differences. An integrated metagenomic and metabolomic analysis further revealed that abundances of several fecal GI metabolites important for nutrient absorption, including three bile acids, correlated with specific microbes in infants with CF. CONCLUSIONS Our results highlight several metagenomic and metabolomic factors, including bile acids and other microbial metabolites, that may impact nutrition, growth, and GI health in infants with CF. These factors could serve as promising avenues for novel microbiome-based therapeutics to improve health outcomes in these infants.
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The gut microbiome in drug-resistant epilepsy.
Chatzikonstantinou, S, Gioula, G, Kimiskidis, VK, McKenna, J, Mavroudis, I, Kazis, D
Epilepsia open. 2021;(1):28-37
Abstract
Drug-resistant epileptic patients make up approximately one-third of the global epilepsy population. The pathophysiology of drug resistance has not been fully elucidated; however, current evidence suggests intestinal dysbiosis, as a possible etiopathogenic factor. Ketogenic diet, whose effect is considered to be mediated by alteration of gut microbiota synthesis, has long been administered in patients with medically refractory seizures, with positive outcomes. In this review, we present data derived from clinical studies regarding alterations of gut microbiome profile in drug-resistant epileptic patients. We further attempt to describe the mechanisms through which the gut microbiome modification methods (including ketogenic diet, pre- or probiotic administration) improve drug-resistant epilepsy, by reporting findings from preclinical and clinical studies. A comprehensive search of the published literature on the PubMed, Embase, and Web of science databases was performed. Overall, the role of gut microbiome in drug-resistant epilepsy is an area which shows promise for the development of targeted therapeutic interventions. More research is required to confirm the results from preliminary studies, as well as safety and effectiveness of altering gut bacterial composition, through the above-mentioned methods.
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The Role of DNA Damage Response in Dysbiosis-Induced Colorectal Cancer.
Rivas-Domínguez, A, Pastor, N, Martínez-López, L, Colón-Pérez, J, Bermúdez, B, Orta, ML
Cells. 2021;(8)
Abstract
The high incidence of colorectal cancer (CRC) in developed countries indicates a predominant role of the environment as a causative factor. Natural gut microbiota provides multiple benefits to humans. Dysbiosis is characterized by an unbalanced microbiota and causes intestinal damage and inflammation. The latter is a common denominator in many cancers including CRC. Indeed, in an inflammation scenario, cellular growth is promoted and immune cells release Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS), which cause DNA damage. Apart from that, many metabolites from the diet are converted into DNA damaging agents by microbiota and some bacteria deliver DNA damaging toxins in dysbiosis conditions as well. The interactions between diet, microbiota, inflammation, and CRC are not the result of a straightforward relationship, but rather a network of multifactorial interactions that deserve deep consideration, as their consequences are not yet fully elucidated. In this paper, we will review the influence of dysbiosis in the induction of DNA damage and CRC.
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Diarrhea Predominant-Irritable Bowel Syndrome (IBS-D): Effects of Different Nutritional Patterns on Intestinal Dysbiosis and Symptoms.
Altomare, A, Di Rosa, C, Imperia, E, Emerenziani, S, Cicala, M, Guarino, MPL
Nutrients. 2021;(5)
Abstract
Irritable Bowel Syndrome (IBS) is a chronic functional gastrointestinal disorder characterized by abdominal pain associated with defecation or a change in bowel habits. Gut microbiota, which acts as a real organ with well-defined functions, is in a mutualistic relationship with the host, harvesting additional energy and nutrients from the diet and protecting the host from pathogens; specific alterations in its composition seem to play a crucial role in IBS pathophysiology. It is well known that diet can significantly modulate the intestinal microbiota profile but it is less known how different nutritional approach effective in IBS patients, such as the low-FODMAP diet, could be responsible of intestinal microbiota changes, thus influencing the presence of gastrointestinal (GI) symptoms. The aim of this review was to explore the effects of different nutritional protocols (e.g., traditional nutritional advice, low-FODMAP diet, gluten-free diet, etc.) on IBS-D symptoms and on intestinal microbiota variations in both IBS-D patients and healthy subjects. To date, an ideal nutritional protocol does not exist for IBS-D patients but it seems crucial to consider the effect of the different nutritional approaches on the intestinal microbiota composition to better define an efficient strategy to manage this functional disorder.
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Gut microbiota in dementia. Critical review of novel findings and their potential application.
Łuc, M, Misiak, B, Pawłowski, M, Stańczykiewicz, B, Zabłocka, A, Szcześniak, D, Pałęga, A, Rymaszewska, J
Progress in neuro-psychopharmacology & biological psychiatry. 2021;:110039
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Abstract
There is a great deal of impetus for the comprehensive understanding of the complete pathological function, genetic information, and functional diversity of the gut microbiota that favors the development of dementia. It has been reported that patients with mild cognitive impairment and Alzheimer's disease present with several metabolic and immune-inflammatory alterations. The recently highlighted aspects of human health linked to cognitive decline include insulin-resistance, obesity, and chronic low-grade inflammation. Gut microbiota is known to produce neurotransmitters, such as GABA, acetylcholine, dopamine or serotonin, vitamins, intestinal toxins, and modulate nerve signaling - with emphasis on the vagus nerve. Additionally, gut dysbiosis results in impaired synthesis of signaling proteins affecting metabolic processes relevant to the development of Alzheimer's disease. Due to numerous links of gut microbiota to crucial metabolic and inflammatory pathways, attempts aimed at correcting the gut microflora composition may affect dementia pathology in a pleiotropic manner. Taking advantage of the metabolic effects of cold exposure on organisms by the introduction of whole-body cryostimulation in dementia patients could lead to alterations in gut microbiota and, therefore, decrease of an inflammatory response and insulin resistance, which remain one of the critical metabolic features of dementia. Further studies are needed in order to explore the potential application of recent findings and ways of achieving the desired goals.
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Intestinal Microbiota as a Contributor to Chronic Inflammation and Its Potential Modifications.
Potrykus, M, Czaja-Stolc, S, Stankiewicz, M, Kaska, Ł, Małgorzewicz, S
Nutrients. 2021;(11)
Abstract
The gut microbiota is a crucial factor in maintaining homeostasis. The presence of commensal microorganisms leads to the stimulation of the immune system and its maturation. In turn, dysbiosis with an impaired intestinal barrier leads to accelerated contact of microbiota with the host's immune cells. Microbial structural parts, i.e., pathogen-associated molecular patterns (PAMPs), such as flagellin (FLG), peptidoglycan (PGN), lipoteichoic acid (LTA), and lipopolysaccharide (LPS), induce inflammation via activation of pattern recognition receptors. Microbial metabolites can also develop chronic low-grade inflammation, which is the cause of many metabolic diseases. This article aims to systematize information on the influence of microbiota on chronic inflammation and the benefits of microbiota modification through dietary changes, prebiotics, and probiotic intake. Scientific research indicates that the modification of the microbiota in various disease states can reduce inflammation and improve the metabolic profile. However, since there is no pattern for a healthy microbiota, there is no optimal way to modify it. The methods of influencing microbiota should be adapted to the type of dysbiosis. Although there are studies on the microbiota and its effects on inflammation, this subject is still relatively unknown, and more research is needed in this area.