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The role of gut microbiome in inflammatory skin disorders: A systematic review.
Widhiati, S, Purnomosari, D, Wibawa, T, Soebono, H
Dermatology reports. 2022;14(1):9188
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Gut-skin axis refers to the complex cross-talk between gut bacteria and skin. Although the exact mechanism underlying chronic inflammatory skin conditions is unknown, imbalances in the composition of gut microbes are believed to play a role. Twenty-three studies were included in this systematic review to assess whether gut microbial imbalance may contribute to inflammatory skin conditions such as Psoriasis, Acne Vulgaris, Atopic Dermatitis, and Urticaria. According to this systematic review, immune stimulation, inflammation, and disruption of bacterial composition are common mechanisms in all these skin disorders. A western diet and environmental exposures are found to be contributing to the disruption of bacteria and the pathology of these skin disorders. It has been observed that friendly gut bacteria such as Bifidobacterium are reduced in people with inflammatory skin conditions, whereas elevated levels of pathogenic bacteria such as E. coli and Proteobacteria are present in the gut of patients with inflammatory skin conditions. The abundance of anti-inflammatory bacteria such as Akkermansia muciniphila, Faecalibacterium prausnitzii, Clostridium leptum, Lactobacillus, and Bifidobacterium may protect against inflammatory skin conditions. Further robust studies are required to evaluate the pathogenesis behind inflammatory skin conditions as well as the involvement of gut bacteria in the development and progression of the disease. Healthcare professionals can gain a deeper understanding of gut bacteria that contribute to the pathology of inflammatory diseases as well as how clinically using anti-inflammatory bacterial species may improve the condition of individuals suffering from inflammatory skin conditions.
Abstract
The close relationship between the intestine and the skin has been widely stated, seen from gastrointestinal (GI) disorders often accompanied by skin manifestations. Exactly how the gut microbiome is related to skin inflammation and influences the pathophysiology mechanism of skin disorders are still unclear. Many studies have shown a two-way relationship between gut and skin associated with GI health and skin homeostasis and allostasis. This systematic review aimed to explore the associations between the gut microbiome with inflammatory skin disorders, such as acne, psoriasis, atopic dermatitis, and urticaria, and to discover the advanced concept of this relationship. The literature search was limited to any articles published up to December 2020 using PubMed and EBSCOHost. The review followed the PRISMA guidelines for conducting a systematic review. Of the 319 articles screened based on title and abstract, 111 articles underwent full-text screening. Of these, 23 articles met our inclusion criteria, comprising 13 atopic dermatitis (AD), three psoriasis, four acne vulgaris, and four chronic urticaria articles. Acne vulgaris, atopic dermatitis, psoriasis, and chronic urticaria are inflammation skin disorders that were studied recently to ascertain the relationship of these disorders with dysbiosis of the GI microbiome. All acne vulgaris, psoriasis, and chronic urticaria studies stated the association of gut microbiome with skin manifestations. However, the results in atopic dermatitis are still conflicting. Most of the articles agree that Bifidobacterium plays an essential role as anti-inflammation bacteria, and Proteobacteria and Enterobacteria impact inflammation in inflammatory skin disorders.
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The Gut Microbiota and Its Implication in the Development of Atherosclerosis and Related Cardiovascular Diseases.
Sanchez-Rodriguez, E, Egea-Zorrilla, A, Plaza-Díaz, J, Aragón-Vela, J, Muñoz-Quezada, S, Tercedor-Sánchez, L, Abadia-Molina, F
Nutrients. 2020;12(3)
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Cardiovascular disease (CVD) is the leading non-communicable disease and cause of death worldwide. The human microbiome can exert direct influences on bodily functions and in recent years much attention has been drawn to the significance of these microorganisms and their role in disease development. Divergences of microbiome patterns are also implicated in the progression and pathogenesis of CVD. This review describes the connection between host microbiota and CVD development. Elaborated are some of the potential mechanisms by which the microbiota and their associated metabolites can directly influence vascular tone and contribute to high blood pressure. More indirect processes, such as microbiota-mediated inflammation, insulin resistance and obesity are also accounted for. Furthermore, the authors discuss modulation of the microbiome composition as potential target for therapeutic interventions. Known influences that alter the microbiome are diet patterns, specific compounds such as probiotics, fish oils and polyphenols, physical activity and novel technologies like faecal transplants. This review outlines the many ways in which the microbiome can contribute to the development of CVD. Summarised are key points to consider in clinical practice, when navigating CVD and its microbiome associated risks factors.
Abstract
The importance of gut microbiota in health and disease is being highlighted by numerous research groups worldwide. Atherosclerosis, the leading cause of heart disease and stroke, is responsible for about 50% of all cardiovascular deaths. Recently, gut dysbiosis has been identified as a remarkable factor to be considered in the pathogenesis of cardiovascular diseases (CVDs). In this review, we briefly discuss how external factors such as dietary and physical activity habits influence host-microbiota and atherogenesis, the potential mechanisms of the influence of gut microbiota in host blood pressure and the alterations in the prevalence of those bacterial genera affecting vascular tone and the development of hypertension. We will also be examining the microbiota as a therapeutic target in the prevention of CVDs and the beneficial mechanisms of probiotic administration related to cardiovascular risks. All these new insights might lead to novel analysis and CVD therapeutics based on the microbiota.
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Melatonin: Roles in influenza, Covid-19, and other viral infections.
Anderson, G, Reiter, RJ
Reviews in medical virology. 2020;30(3):e2109
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Viruses like influenza and coronaviruses change quickly, making it challenging to develop effective treatments and vaccines in a short time frame. Consequently, the use of generic substances that limit viral effects are of high interest. In this paper, the authors summarize a range of mechanisms in which melatonin can alter the impact of virus infections and infection-associated inflammatory overdrive aka cytokine storm. Melatonin, the sleep hormone, is well known for its potent antioxidant and anti-inflammatory action. It seems highly likely that melatonin can modulate the cellular function of all cells, mostly via mitochondrial function. This is particularly relevant in immune cells. For example, the daytime variance in immune function seems to be closely linked with mitochondrial activity and energy production. Other relevant mechanisms described are the antiviral role of melatonin-induced sirtuins - proteins that regulate cellular health-, the impact of viruses on cell coordinating microRNA, the role of the gut microbiome and gut permeability, as well as sympathetic nervous system activation and the protective effects of parasympathetic activation. Also considered are pre-existing health conditions and conditions that are linked with a decline in melatonin along with ageing, all being groups in which severity of viral infections is felt. This paper may be of interest to those who like to explore in more depth the mechanisms behind melatonin and its ability to influence viral disease progression.
Abstract
There is a growing appreciation that the regulation of the melatonergic pathways, both pineal and systemic, may be an important aspect in how viruses drive the cellular changes that underpin their control of cellular function. We review the melatonergic pathway role in viral infections, emphasizing influenza and covid-19 infections. Viral, or preexistent, suppression of pineal melatonin disinhibits neutrophil attraction, thereby contributing to an initial "cytokine storm", as well as the regulation of other immune cells. Melatonin induces the circadian gene, Bmal1, which disinhibits the pyruvate dehydrogenase complex (PDC), countering viral inhibition of Bmal1/PDC. PDC drives mitochondrial conversion of pyruvate to acetyl-coenzyme A (acetyl-CoA), thereby increasing the tricarboxylic acid cycle, oxidative phosphorylation, and ATP production. Pineal melatonin suppression attenuates this, preventing the circadian "resetting" of mitochondrial metabolism. This is especially relevant in immune cells, where shifting metabolism from glycolytic to oxidative phosphorylation, switches cells from reactive to quiescent phenotypes. Acetyl-CoA is a necessary cosubstrate for arylalkylamine N-acetyltransferase, providing an acetyl group to serotonin, and thereby initiating the melatonergic pathway. Consequently, pineal melatonin regulates mitochondrial melatonin and immune cell phenotype. Virus- and cytokine-storm-driven control of the pineal and mitochondrial melatonergic pathway therefore regulates immune responses. Virus-and cytokine storm-driven changes also increase gut permeability and dysbiosis, thereby suppressing levels of the short-chain fatty acid, butyrate, and increasing circulating lipopolysaccharide (LPS). The alterations in butyrate and LPS can promote viral replication and host symptom severity via impacts on the melatonergic pathway. Focussing on immune regulators has treatment implications for covid-19 and other viral infections.
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Gut microbial metabolites in depression: understanding the biochemical mechanisms.
Caspani, G, Kennedy, S, Foster, JA, Swann, J
Microbial cell (Graz, Austria). 2019;6(10):454-481
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Major depressive disorder is a leading cause of disability and is linked to shortened life expectancy and suicide. Despite its prevalence, for near to a third of patients, long-term treatment options are ineffective. In addition to the primary presentation of persistent low mood, other emotional and physiological symptoms, researchers have also identified alterations in metabolism, hormones and the immune system. Furthermore, increasing evidence suggests that depression and depressive behaviour is also influenced by divergences in gut health and gut bacteria composition. With insights from animal and human research, this review highlights how the gut and gut bacteria-derived metabolites can directly or indirectly influence mood. Described are the pathways of how the gut and its microorganism communicate with the brain, the essential role the immune system has as part of the gut-brain communication, and the impact of low-grade, chronic inflammation on neurofunction. Comprehensive summaries are dedicated to how several metabolites or by-products from gut bacteria can influence the nervous system and gene expression in relation to depression. These include substances like neurotransmitters, short-chain fatty acids, tryptophan metabolites, lactate, bile acids, choline metabolites and folate. This article yields a detailed overview of how gut health and microbiota can influence neurofunction and mental health. The authors promote the idea of the gut as a suitable target for the management of depressive disorders, whilst also eluding to the current limitations and need for further research.
Abstract
Gastrointestinal and central function are intrinsically connected by the gut microbiota, an ecosystem that has co-evolved with the host to expand its biotransformational capabilities and interact with host physiological processes by means of its metabolic products. Abnormalities in this microbiota-gut-brain axis have emerged as a key component in the pathophysiology of depression, leading to more research attempting to understand the neuroactive potential of the products of gut microbial metabolism. This review explores the potential for the gut microbiota to contribute to depression and focuses on the role that microbially-derived molecules - neurotransmitters, short-chain fatty acids, indoles, bile acids, choline metabolites, lactate and vitamins - play in the context of emotional behavior. The future of gut-brain axis research lies is moving away from association, towards the mechanisms underlying the relationship between the gut bacteria and depressive behavior. We propose that direct and indirect mechanisms exist through which gut microbial metabolites affect depressive behavior: these include (i) direct stimulation of central receptors, (ii) peripheral stimulation of neural, endocrine, and immune mediators, and (iii) epigenetic regulation of histone acetylation and DNA methylation. Elucidating these mechanisms is essential to expand our understanding of the etiology of depression, and to develop new strategies to harness the beneficial psychotropic effects of these molecules. Overall, the review highlights the potential for dietary interventions to represent such novel therapeutic strategies for major depressive disorder.
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Small talk: microbial metabolites involved in the signaling from microbiota to brain.
Caspani, G, Swann, J
Current opinion in pharmacology. 2019;48:99-106
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The gut-brain axis (GBA) is the communication network between the gastrointestinal tract and the central nervous system. An array of gut bacteria-derived metabolites mediates this interaction between the gastrointestinal system and the brain, influencing physiological and pathological processes in direct and indirect ways. Thus a variation in the gut microbiome can alter the functional capacity and output of the gut-brain-communication. In this review, the authors summarise key bacterial metabolites from the gut and their effect on the brain. Addressed are short-chain fatty acids, their impact on gut and brain barrier integrity, their role in appetite regulation, and their association with anxiety and depressive disorders amongst other aspects. Secondly, bile acids, which are processed by the microbiome, can activate several receptors. And thus divergence gut bacteria can alter the composition of bile acids and change their signalling capacity. Bile acids can also directly modify gut and blood-brain barrier function and may carry a signalling role in the brain. A few neurotransmitters are covered in this article, as several types of gut bacteria synthesize neurotransmitters, such as serotonin and dopamine. Though, it is uncertain whether all gut-derived neurotransmitters can reach the brain. However, certain GABA-producing bacteria have been shown to elicit higher GABA levels in the brain. The microbiota can also be involved with the conversion of neurotransmitters such as dopamine. The final section briefly capture the evidence of other brain health-relevant molecules derived from the intestinal microbiota, including Lipopolysaccharides, choline, lactate and B-Vitamins. This review yields a short and comprehensive summary highlighting the many ways the gut can influence brain function and health and could be of interest to those providing mental health support in light of gut function.
Abstract
The wealth of biotransformational capabilities encoded in the microbiome expose the host to an array of bioactive xenobiotic products. Several of these metabolites participate in the communication between the gastrointestinal tract and the central nervous system and have potential to modulate central physiological and pathological processes. This biochemical interplay can occur through various direct and indirect mechanisms. These include binding to host receptors in the brain, stimulation of the vagus nerve in the gut, alteration of central neurotransmission, and modulation of neuroinflammation. Here, the potential for short chain fatty acids, bile acids, neurotransmitters and other bioactive products of the microbiome to participate in the gut-brain axis will be reviewed.
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Crosstalk between the microbiome and epigenome: messages from bugs.
Qin, Y, Wade, PA
Journal of biochemistry. 2018;163(2):105-112
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Trillions of microbes live symbiotically in and on an individual human being, most of them inside the digestive tract and communally known as the gut microbiome. The gut microbiome plays a vital role in the individual host’s health, not only by helping digest food and harvest energy, but also by regulating immune development and influencing gene expression. Diet and factors, such as infections and the use of antibiotics, can alter the balance of the microbiome and lead to various outcomes. This paper reviewed the current understanding of the ways in which the gut microbiome is capable of altering the host’s gene expression through microbial signals, including metabolites, bile acids, inflammation and altered composition. The studies highlighted in the paper show that gut microbes communicate both with local cells in the intestines and with more distant organs, such as the liver and the cardiovascular system. Through this communication, they can regulate the expression of immune cells, cancer cells, enzymes and inflammation-related molecules. The authors concluded that these interactions, or the crosstalk between the microbes and the host, demonstrate a crucial role of the gut microbiome in the host’s response to environmental signals. However, many of the mechanisms are still unclear, so further studies are needed to explain specific microbe-derived signals, affecting host gene expression, and to deepen our understanding of how lifestyle, health status and environmental exposures, such as antibiotics, regulate the microbiome and its influence.
Abstract
Mammals exist in a complicated symbiotic relationship with their gut microbiome, which is postulated to have broad impacts on host health and disease. As omics-based technologies have matured, the potential mechanisms by which the microbiome affects host physiology are being addressed. The gut microbiome, which provides environmental cues, can modify host cell responses to stimuli through alterations in the host epigenome and, ultimately, gene expression. Increasing evidence highlights microbial generation of bioactive compounds that impact the transcriptional machinery in host cells. Here, we review current understanding of the crosstalk between gut microbiota and the host epigenome, including DNA methylation, histone modification and non-coding RNAs. These studies are providing insights into how the host responds to microbial signalling and are predicted to provide information for the application of precision medicine.
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Physical exercise, gut, gut microbiota, and atherosclerotic cardiovascular diseases.
Chen, J, Guo, Y, Gui, Y, Xu, D
Lipids in health and disease. 2018;17(1):17
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Cardiovascular diseases (CVD), such as heart attacks and strokes, are the leading cause for mortality worldwide. Many studies have shown beneficial effects of physical exercise on cardiovascular risk factors, such as high cholesterol, high blood pressure, abdominal obesity and diabetes. However, some of the mechanisms, by which these beneficial effects occur, are not well understood. It is believed that gut microbiota, affected by physical exercise, altering the intestinal environment, plays a role. This review paper summarised the current understanding on the effects of physical exercise on CVD, through its effects on the gut microbiota and intestinal function. The authors reviewed animal and human studies looking at how various types of exercise, such as high-intensity interval training (mice), running (rats and mice) and rugby (humans), affect diversity and distribution of microbes, metabolites produced by microbiota, intestinal wall integrity and systemic inflammation. Based on the reviewed papers, the authors concluded that, although further research is warranted, many studies confirm the premise that physical exercise can prevent CVD through modifying gut microbiota and alleviating systemic inflammation.
Abstract
Arteriosclerotic cardiovascular diseases (ASCVDs) are the leading cause of morbidity and mortality worldwide and its risk can be independently decreased by regular physical activity. Recently, ASCVD and its risk factors were found to be impacted by the gut microbiota through its diversity, distribution and metabolites. Meanwhile, several experiments demonstrated the relationship between physical exercise and diversity, distribution, metabolite of the gut microbiota as well as its functions on the lipid metabolism and chronic systematic inflammation. In this review, we summarize the current knowledge on the effects of physical exercise on ASCVD through modulation of the gut microbiota and intestinal function.
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L-carnitine ameliorated fasting-induced fatigue, hunger, and metabolic abnormalities in patients with metabolic syndrome: a randomized controlled study.
Zhang, JJ, Wu, ZB, Cai, YJ, Ke, B, Huang, YJ, Qiu, CP, Yang, YB, Shi, LY, Qin, J
Nutrition journal. 2014;13:110
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Metabolic syndrome increases the risk of heart disease and diabetes. Modified fasting therapy, such as a very-low-calorie diet is considered an effective way to tackle obesity and metabolic syndrome. When fasting, calorie restriction may cause fatigue and intense hunger, which may tempt individuals to stop fasting. L-Carnitine is an amino acid that transports long-chain fatty acids to mitochondria and helps them be oxidised to produce energy. L-Carnitine intravenous therapy is more bioavailable, better absorbed, and cleared than oral supplementation. This randomised, single-blinded, placebo-controlled pilot study included 30 individuals with metabolic syndrome who were randomly assigned to receive either 4 g/day of intravenous L-carnitine or saline for seven days to evaluate the effect of L-Carnitine on fatigue, hunger, body mass, lipid profile, and other CHD risk factors during a modified fasting period. The L-Carnitine group showed a significant reduction in waist-hip ratio, body mass, serum insulin levels, γ-glutamyltransferase, mental and physical fatigue, fatigue severity, weight loss, and greater reduction in waist circumference, total cholesterol and hunger when compared to the control group. Healthcare professionals can use the results of this study to understand the beneficial effects of L-Carnitine administration during modified fasting therapy in reducing weight, metabolic risk factors, hunger and fatigue. Long-term studies are required to confirm the benefits of L-carnitine.
Abstract
BACKGROUND The present study aimed to determine that whether L-carnitine infusion could ameliorate fasting-induced adverse effects and improve outcomes. METHOD In this 7-day, randomized, single-blind, placebo-controlled, pilot study, 15 metabolic syndrome (MetS) patients (11/4 F/M; age 46.9 ± 9.14 years; body mass index [BMI] 28.2 ± 1.8 kg/m2) were in the L-carnitine group (LC) and 15 (10/5 F/M; age 46.8 ± 10.9 years; BMI 27.1 ± 2.3 kg/m2) were in the control group (CT). All participants underwent a 5-day modified fasting therapy introduced with 2-day moderate calorie restriction. Patients in the LC group received 4 g/day of intravenous L-carnitine, while patients in the CT group were injected with saline. Blood pressure (BP), anthropometric characteristics, markers of liver function, metabolic indices (plasma glucose, lipid profiles, uric acid, free fatty acid and insulin) and hypersensitivity C-reactive protein were measured. Perceived hunger was recorded daily by self-rating visual analogue scales. Fatigue was evaluated by Wessely and Powell scores. RESULTS In contrast to the CT group, total cholesterol, alanine aminotransferase, systolic and diastolic BP did not change significantly in the LC group after prolonged fasting. There were significant differences in weight loss (LC -4.6 ± 0.9 vs. CT -3.2 ± 1.1 kg, P = 0.03), and waist circumference (LC -5.0 ± 2.2 vs. CT -1.7 ± 1.16 cm, P < 0.001), waist hip ratio (LC -0.023 ± 0.017 vs. CT 0.012 ± 0.01, P < 0.001), insulin concentration (LC -9.9 ± 3.58 vs. CT -6.32 ± 3.44 µU/mL, P = 0.046), and γ-glutamyltransferase concentration (LC -7.07 ± 6.82 vs. CT -2.07 ± 4.18, P = 0.024). Perceived hunger scores were significantly increased (P < 0.05) in the CT group during starvation, which was alleviated with L-carnitine administration in the LC group. Physical fatigue (LC -3.2 ± 3.17 vs. CT 1.8 ± 2.04, P < 0.001) and fatigue severity (LC -11.6 ± 8.38 vs. CT 8.18 ± 7.32, P < 0.001) were significantly reduced in the LC group but were aggravated in the CT group. CONCLUSION Intravenous L-carnitine can ameliorate fasting-induced hunger, fatigue, cholesterol abnormalities and hepatic metabolic changes and facilitate fasting-induced weight loss in MetS patients. TRIAL REGISTRATION ChiCTR-TNRC-12002835.