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Metabolomics has come to the fore as an efficient tool in the search for biomarkers that are critical for precision health approaches and improved diagnostics. This review will outline recent advances in biomarker discovery based on metabolomics, focusing on metabolomics biomarkers reported in cancer, neurodegenerative disorders, cardiovascular diseases, and metabolic health. In cancer, metabolomics provides evidence for unique oncometabolites that are important for early disease detection and monitoring of treatment responses. Metabolite profiling for conditions such as neurodegenerative and mental health disorders can offer early diagnosis and mechanisms into the disease especially in Alzheimer's and Parkinson's diseases. In addition to these, lipid biomarkers and other metabolites relating to cardiovascular and metabolic disorders are promising for patient stratification and personalized treatment. The gut microbiome and environmental exposure also feature among the influential factors in biomarker discovery because they sculpt individual metabolic profiles, impacting overall health. Further, we discuss technological advances in metabolomics, current clinical applications, and the challenges faced by metabolomics biomarker validation toward precision medicine. Finally, this review discusses future opportunities regarding the integration of metabolomics into routine healthcare to enable preventive and personalized approaches. [ABSTRACT FROM AUTHOR]

Background: Several randomized controlled trials (RCTs) have shown conflicting results on cortisol levels following probiotic administration in healthy and diseased populations. Previous analyses were inconclusive due to limited studies, and evidence is lacking on how these effects vary by health status; region; therapy duration; medications, and use of single or multiple strains. Methods: In this systematic review and meta-analysis (PROSPERO [CRD42024538539]), we searched PubMed, Cochrane Library, Embase, Scopus, Web of Science, CINAHL, ProQuest, and Web of Science Preprints until 13 August 2024, for RCTs on probiotic administration, either alone or combined, across all age groups and without specific medical condition requirements. We applied random-effects meta-analysis, assessed bias using the Cochrane RoB 2 tool, and evaluated evidence certainty with GRADE. Findings: We screened 1739 records and retrieved 46 RCTs (3516 participants). Probiotics supplementation decreased cortisol levels compared to the control arm [46 RCTs; SMD: −0.45; 95% CI: −0.83; −0.07; I2: 92.5%, low certainty]. Among various subgroups; probiotics supplementation decreased the cortisol levels in the subgroups without concomitant medications [37 RCTs; SMD: −0.30; 95% CI [−0.58; −0.03], I2: 88.7%] with a single probiotic strain [30 RCTs; SMD: −0.33; 95% CI: −0.63; −0.028; I2: 88.8%], in a healthy population [35 RCTs; SMD:−0.3; 95% CI: −0.58; −0.03; I2: 88.7] and in the Asia region [21 RCTs; SMD: −0.83; 95% CI: −1.58; −0.07; I2: 95%]. Interpretation: A low level of evidence suggests probiotics might reduce cortisol levels, but more targeted studies are needed to identify variables affecting the response in specific subgroups. [ABSTRACT FROM AUTHOR]

Background: Heat stress (HS) commonly occurs as a severe pathological response when the body's sensible temperature exceeds its thermoregulatory capacity, leading to the development of chronic brain inflammation, known as neuroinflammation. Emerging evidence suggests that HS leads to the disruption of the gut microbiota, whereas abnormalities in the gut microbiota have been demonstrated to affect neuroinflammation. However, the mechanisms underlying the effects of HS on neuroinflammation are poorly studied. Meanwhile, effective interventions have been unclear. β‐Hydroxybutyric acid (BHBA) has been found to have neuroprotective and anti‐inflammatory properties in previous studies. This study aims to explore the modulatory effects of BHBA on neuroinflammation induced by HS and elucidate the underlying molecular mechanisms. Methods: An in vivo and in vitro model of HS was constructed under the precondition of BHBA pretreatment. The modulatory effects of BHBA on HS‐induced neuroinflammation were explored and the underlying molecular mechanisms were elucidated by flow cytometry, WB, qPCR, immunofluorescence staining, DCFH‐DA fluorescent probe assay, and 16S rRNA gene sequencing of colonic contents. Results: Heat stress was found to cause gut microbiota disruption in HS mouse models, and TM7 and [Previotella] spp. may be the best potential biomarkers for assessing the occurrence of HS. Fecal microbiota transplantation associated with BHBA effectively reversed the disruption of gut microbiota in HS mice. Moreover, BHBA may inhibit microglia hyperactivation, suppress neuroinflammation (TNF‐α, IL‐1β, and IL‐6), and reduce the expression of cortical endoplasmic reticulum stress (ERS) markers (GRP78 and CHOP) mainly through its modulatory effects on the gut microbiota (TM7, Lactobacillus spp., Ruminalococcus spp., and Prevotella spp.). In vitro experiments revealed that BHBA (1 mM) raised the expression of the ERS marker GRP78, enhanced cellular activity, and increased the generation of reactive oxygen species (ROS) and anti‐inflammatory cytokines (IL‐10), while also inhibiting HS‐induced apoptosis, ROS production, and excessive release of inflammatory cytokines (TNF‐α and IL‐1β) in mouse BV2 cells. Conclusion: β‐Hydroxybutyric acid may be an effective agent for preventing neuroinflammation in HS mice, possibly due to its ability to inhibit ERS and subsequent microglia neuroinflammation via the gut–brain axis. These findings lay the groundwork for future research and development of BHBA as a preventive drug for HS and provide fresh insights into techniques for treating neurological illnesses by modifying the gut microbiota. [ABSTRACT FROM AUTHOR]

Metastatic disease, a leading and lethal indication of deaths associated with tumors, results from the dissemination of metastatic tumor cells from the site of primary origin to a distant organ. Dispersion of metastatic cells during the development of tumors at distant organs leads to failure to comply with conventional treatments, ultimately instigating abrupt tissue homeostasis and organ failure. Increasing evidence indicates that the tumor microenvironment (TME) is a crucial factor in cancer progression and the process of metastatic tumor development at secondary sites. TME comprises several factors contributing to the initiation and progression of the metastatic cascade. Among these, various cell types in TME, such as mesenchymal stem cells (MSCs), lymphatic endothelial cells (LECs), cancer-associated fibroblasts (CAFs), myeloid-derived suppressor cells (MDSCs), T cells, and tumor-associated macrophages (TAMs), are significant players participating in cancer metastasis. Besides, various other factors, such as extracellular matrix (ECM), gut microbiota, circadian rhythm, and hypoxia, also shape the TME and impact the metastatic cascade. A thorough understanding of the functions of TME components in tumor progression and metastasis is necessary to discover new therapeutic strategies targeting the metastatic tumor cells and TME. Therefore, we reviewed these pivotal TME components and highlighted the background knowledge on how these cell types and disrupted components of TME influence the metastatic cascade and establish the premetastatic niche. This review will help researchers identify these altered components' molecular patterns and design an optimized, targeted therapy to treat solid tumors and restrict metastatic cascade. [ABSTRACT FROM AUTHOR]

To improve performance and recovery faster, athletes are advised to eat more often than usual and consume higher doses of simple carbohydrates, during and after exercise. Sports energetic supplements contain food additives, such as artificial sweeteners, emulsifiers, acidity regulators, preservatives, and salts, which could be harmful to the gut microbiota and impair the intestinal barrier function. The intestinal barrier plays a critical function in bidirectionally regulation of the selective transfer of nutrients, water, and electrolytes, while preventing at the same time, the entrance of harmful substances (selective permeability). The gut microbiota helps to the host to regulate intestinal homeostasis through metabolic, protective, and immune functions. Globally, the gut health is essential to maintain systemic homeostasis in athletes, and to ensure proper digestion, metabolization, and substrate absorption. Gastrointestinal complaints are an important cause of underperformance and dropout during endurance events. These complications are directly related to the loss of gut equilibrium, mainly linked to microbiota dysbiosis and leaky gut. In summary, athletes must be cautious with the elevated intake of ultra-processed foods and specifically those contained on sports nutrition supplements. This review points out the specific nutritional interventions that should be implemented and/or discontinued depending on individual gut functionality. [ABSTRACT FROM AUTHOR]

With new advances in next generation sequencing (NGS) technology at reduced costs, research on bacterial genomes in the environment has become affordable. Compared to traditional methods, NGS provides high-throughput sequencing reads and the ability to identify many species in the microbiome that were previously unknown. Numerous bioinformatics tools and algorithms have been developed to conduct such analyses. However, in order to obtain biologically meaningful results, the researcher must select the proper tools and combine them to construct an efficient pipeline. This complex procedure may include tens of tools, each of which require correct parameter settings. Furthermore, an NGS data analysis involves multiple series of command-line tools and requires extensive computational resources, which imposes a high barrier for biologists and clinicians to conduct NGS analysis and even interpret their own data. Therefore, we established a public gut microbiome database, which we call Twnbiome, created using healthy subjects from Taiwan, with the goal of enabling microbiota research for the Taiwanese population. Twnbiome provides users with a baseline gut microbiome panel from a healthy Taiwanese cohort, which can be utilized as a reference for conducting case-control studies for a variety of diseases. It is an interactive, informative, and user-friendly database. Twnbiome additionally offers an analysis pipeline, where users can upload their data and download analyzed results. Twnbiome offers an online database which non-bioinformatics users such as clinicians and doctors can not only utilize to access a control set of data, but also analyze raw data with a few easy clicks. All results are customizable with ready-made plots and easily downloadable tables. Database URL: http://twnbiome.cgm.ntu.edu.tw/. [ABSTRACT FROM AUTHOR]

This study aimed to isolate and characterize probiotic Lactobacilli from human faecal samples of Jammu region of India and evaluation of their antioxidative properties. A total of 29 Lactobacillus strains were isolated and tested for their ability to withstand different pH levels, high concentrations of bile salt and lysozyme along with their adhesion ability to different hydrocarbons and auto-aggregation. Selected probiotic Lactobacillus isolates were further examined for their antioxidant potential using ABTS, DPPH methods, and the ability to scavenge superoxide and hydroxyl radicals. The results showed that Lactobacillus LpJ1 (7.93 ± 0.23) and LpJ5 (7.93 ± 0.59) had the highest cell viability at a pH of 2.5, while Lactobacillus LpJ16 (7.91 ± 0.48) had the highest resistance to bile salts. Many of the isolates also demonstrated good tolerance to lysozyme. The adhesion abilities of these isolates were characterized by cell surface hydrophobicity and auto aggregation which ranged between 50.32% to 77.8% and 51.02% to 78.95% respectively. In addition, Lactobacillus LpJ5 and LpJ8 showed excellent antioxidant activity. Based on these findings, the selected probiotic strains could be potential candidates for use in functional food to reduce oxidative stress. [ABSTRACT FROM AUTHOR]

Obesity is a complex health condition that increases the susceptibility to developing cardiovascular diseases, diabetes, and numerous other metabolic health issues. The effect of obesity is not just limited to the conditions mentioned above; it is also seen to have a profound impact on the patient's mental state, leading to the onset of various mental disorders, particularly mood disorders. Therefore, it is necessary to understand the mechanism underlying the crosstalk between obesity and mental disorders. The gut microbiota is vital in regulating and maintaining host physiology, including metabolism and neuronal circuits. Because of this newly developed understanding of gut microbiota role, here we evaluated the published diverse information to summarize the achievement in the field. In this review, we gave an overview of the association between obesity, mental disorders, and the role of gut microbiota there. Further new guidelines and experimental tools are necessary to understand the microbial contribution to regulate a balanced healthy life. [ABSTRACT FROM AUTHOR]

Metabolic-dysfunction-associated fatty-liver disease (MAFLD) is the principal worldwide cause of liver disease. Individuals with nonalcoholic steatohepatitis (NASH) have a higher prevalence of small-intestinal bacterial overgrowth (SIBO). We examined gut-microbiota isolated from 12-week-old stroke-prone spontaneously hypertensive-5 rats (SHRSP5) fed on a normal diet (ND) or a high-fat- and high-cholesterol-containing diet (HFCD) and clarified the differences between their gut-microbiota. We observed that the Firmicute/Bacteroidetes (F/B) ratio in both the small intestines and the feces of the SHRSP5 rats fed HFCD increased compared to that of the SHRSP5 rats fed ND. Notably, the quantities of the 16S rRNA genes in small intestines of the SHRSP5 rats fed HFCD were significantly lower than those of the SHRSP5 rats fed ND. As in SIBO syndrome, the SHRSP5 rats fed HFCD presented with diarrhea and body-weight loss with abnormal types of bacteria in the small intestine, although the number of bacteria in the small intestine did not increase. The microbiota of the feces in the SHRSP5 rats fed HFCD was different from those in the SHRP5 rats fed ND. In conclusion, there is an association between MAFLD and gut-microbiota alteration. Gut-microbiota alteration may be a therapeutic target for MAFLD. [ABSTRACT FROM AUTHOR]

Gut microbiota regulates essential processes of host metabolism and physiology: synthesis of vitamins, digestion of foods non-digestible by the host (such as fibers), and—most important—protects the digestive tract from pathogens. In this study, we focus on the CRISPR/Cas9 technology, which is extensively used to correct multiple diseases, including liver diseases. Then, we discuss the non-alcoholic fatty liver disease (NAFLD), affecting more than 25% of the global population; colorectal cancer (CRC) is second in mortality. We give space to rarely discussed topics, such as pathobionts and multiple mutations. Pathobionts help to understand the origin and complexity of the microbiota. Since several types of cancers have as target the gut, it is vital extending the research of multiple mutations to the type of cancers affecting the gut–liver axis. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease (IBD) is the most common form of intestinal inflammation associated with a dysregulated immune system response to the commensal microbiota in a genetically susceptible host. IBD includes ulcerative colitis (UC) and Crohn's disease (CD), both of which are remarkably heterogeneous in their clinical presentation and response to treatment. This translates into a notable diagnostic challenge, especially in underdeveloped countries where IBD is on the rise and access to diagnosis or treatment is not always accessible for chronic diseases. The present work characterized, for the first time in our region, epigenetic biomarkers and gut microbial profiles associated with UC and CD patients in the Buenos Aires Metropolitan area and revealed differences between non-IBD controls and IBD patients. General metabolic functions associated with the gut microbiota, as well as core microorganisms within groups, were also analyzed. Additionally, the gut microbiota analysis was integrated with relevant clinical, biochemical and epigenetic markers considered in the follow-up of patients with IBD, with the aim of generating more powerful diagnostic tools to discriminate phenotypes. Overall, our study provides new insights into data analysis algorithms to promote comprehensive phenotyping tools using quantitative and qualitative analysis in a transkingdom interactions network context. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease (IBD) is the most common form of intestinal inflammation associated with a dysregulated immune system response to the commensal microbiota in a genetically susceptible host. IBD includes ulcerative colitis (UC) and Crohn's disease (CD), both of which are remarkably heterogeneous in their clinical presentation and response to treatment. This translates into a notable diagnostic challenge, especially in underdeveloped countries where IBD is on the rise and access to diagnosis or treatment is not always accessible for chronic diseases. The present work characterized, for the first time in our region, epigenetic biomarkers and gut microbial profiles associated with UC and CD patients in the Buenos Aires Metropolitan area and revealed differences between non-IBD controls and IBD patients. General metabolic functions associated with the gut microbiota, as well as core microorganisms within groups, were also analyzed. Additionally, the gut microbiota analysis was integrated with relevant clinical, biochemical and epigenetic markers considered in the follow-up of patients with IBD, with the aim of generating more powerful diagnostic tools to discriminate phenotypes. Overall, our study provides new insights into data analysis algorithms to promote comprehensive phenotyping tools using quantitative and qualitative analysis in a transkingdom interactions network context. [ABSTRACT FROM AUTHOR]

Human body is colonized by a complex ecosystem of microbes that play a significant role in determining the fitness of the host. The epigenetic signatures of probiotic microorganisms also define the functional role of microbiota in the intestine and further facilitate exploring their beneficial properties. Development in the areas of molecular biology and genomics has paved way for engineering of microorganisms. The advent of genome editing tools such as CRISPR-Cas, has revolutionized new possibilities for genetic engineering in probiotics for enhanced immune response, antimicrobial properties and applications in biotherapeutics. Here, we discuss the present status of genome editing used in epigenome engineering of the gut microbiota and role of different types of CRISPR-Cas systems. Applications of CRISPR-Cas system can be harnessed to modify probiotic microbes in order to regulate gene expressions and produce desired metabolite. These techniques illuminate novel approaches to metabolic engineering and draw attention towards poorly characterized biosynthetic pathways. In addition, future prospects of these tools can be applied to investigate the interactions between gut microbiome and the host, hence, contributing to the development of novel therapeutics. [ABSTRACT FROM AUTHOR]

Respiratory diseases are responsible for a greater mortality rate around the world. Viral or bacterial infections in the respiratory tract have been identified as major causative agents for death and disability among the population. Respiratory tract infections (RTIs) cause severe respiratory ailments starting from coldlike symptoms, eventually affecting the lungs and other viscera, and are mainly categorized into two types depending on the affected area: upper RTIs and lower RTIs. Respiratory viruses belong to several viral families such as influenza virus, enterovirus, adenovirus, respiratory syncytial virus, and recently severe acute respiratory syndrome coronavirus 2. Studies have indicated that people with good immune functions are less prone to respiratory infections and also their recovery rate is quicker. Innate and acquired immune systems actively participate in the recognition and elimination of the pathogenic agents. In the present context, the potential of probiotics is recognized as viable microorganisms that support the balance of the beneficial microbial population in the gastrointestinal tract and promote host immunity. The probiotics have long been known to regulate bodily immune functions and have been used against general RTIs such as cough, pharyngitis, laryngitis, pneumonia, and asthma. In addition, intervention with probiotics could directly affect the composition of the gut microbiota that have been shown to palliate respiratory diseases by modulating pulmonary immune activities through the gut–lung axis, and therefore, probiotics could become an alternative therapeutic approach for RTIs. [ABSTRACT FROM AUTHOR]

Aflatoxin B1 (AFB1) induced intestinal epithelial damage in rodent models, which indicates that long-term exposure to AFB1 may cause chronic gut disorders. In this study, we tested the hypothesis that AFB1-induced adverse effects on gut is mediated by gut-microbiota, which is partially reflected by the changes of fecal microbiome and metabolome. F344 rats were orally exposed to AFB1 of 0, 5, 25, and 75 µg kg−1 body weight for 4 weeks and fecal samples were collected. An ion-fragmentation-spectrum-based metabolomics approach was developed to investigate the fecal microbiota-associated metabolic changes in fecal samples. We found that AFB1 inhibited the hepatic and intestinal metabolism of bile constituents. As compared with the controls, bile acid synthesis-associated cholesterols in rats treated with 25 µg kg−1 (the middle-dose group) were significantly decreased in the fecal samples, for example, lathosterol (45% reduction), cholesterol ester (21% reduction), chenodeoxycholic acid (20% reduction), dihydroxycholesterol (55% reduction), hydroxycholesterol (20% reduction), and 5-cholestene (29% reduction). Although disease-associated lipids were not detectable in the feces of the control group, they were found in AFB1-treated groups, including diglyceride, monoacylglyceride, 19,20-dihydroxy-docosapentaenoic acid, and phosphatidylethanolamine. Metabolisms of carbohydrates and production of short-chain fatty acids were remarkedly decreased in all treated groups. Moreover, an inflammatory-bowel-disease (IBD)-associated taxonomic structure of fecal microbiota was observed as ∼25% Lachnospiraceae , ∼25% Ruminococcaceae , and <1% Lactobacillales , which was similar to the composition pattern found in IBD patients. These results suggest that AFB1-induced disruption on gut-microbiota, partially reflected by fecal microbiome and metabolome, may play important roles in the pathogenesis of chronic gut disorders. [ABSTRACT FROM AUTHOR]

Alzheimer’s disease is neurodegenerative dementia which has significant health complications in the old age group. An imbalance in gut microbiota can influence to cause several diseases like chronic disorders, depression, type II diabetics, and neurological disorders like AD. Aging is one of the major causes of the development of neurodegenerative disease due to the decreasing levels of neurotransmitters, oxidative stress, chronic inflammation, and apoptosis. These harmful effects of aging can be prevented by probiotics usage. The gut-microbiota is capable to control the brain function through the gut-brain axis. Lactobacillus strains are considered as beneficial microorganism because of its importance of the maintenance in healthy intestinal microflora, immunomodulation, and intestinal pathogenic intervention. They have diverse applications in the medical field with properties like antioxidant, anticancer, anti-inflammatory, anti-proliferative, anti-obesity, and anti-diabetic activities. Probiotic supplementation with Lactobacillus strains shows an optimistic trend to use it as a significant therapy for cognitive symptoms. This review article put forwards the significance of the gut-brain axis and the contribution of Lactobacillus strains as a probiotic supplement and its therapeutic innovations for future aspects and the limitation to treat AD-related pathogenesis are briefly elucidated. [ABSTRACT FROM AUTHOR]

An association between gut–microbiota and several neuropsychiatric conditions including autism, depression, anxiety, schizophrenia, and attention-deficit/hyperactivity disorder (ADHD) has been observed. Despite being the most prevalent neurodevelopmental disorders in children and adolescents worldwide, the etiology and curative approaches to treatment of ADHD remain unclear. There is a probability that gut–microbiota may contribute to ADHD via bidirectional communication between the gut and brain, a system known as the "gut–brain axis". Although a mechanistic link in the gut–brain axis in ADHD has been proposed, there is still a lack of information about the correlation of the microbiome profile with the mechanisms involved. The objective of this review was to summarize the diversity of the gut–microbiota and taxonomic profiles in children and adolescents with ADHD. In this review, we have provided an overview of the association between ADHD and gut–microbiota. The evidence pertinent to potentially distinctive gut–microbiota in children and adolescents with ADHD is also discussed and compared to that of their non-ADHD peers. Finally, the implications and future directions for investigation into the gut microbiome in ADHD patients are proposed. [ABSTRACT FROM AUTHOR]

The endocannabinoid system (ECS) has emerged in recent years as a potential treatment target for alcohol use disorders (AUD). In particular, the nonpsychoactive cannabinoid cannabidiol (CBD) has shown preclinical promise in ameliorating numerous clinical symptoms of AUD. There are several proposed mechanism(s) through which cannabinoids (and CBD in particular) may confer beneficial effects in the context of AUD. First, CBD may directly impact specific brain mechanisms underlying AUD to influence alcohol consumption and the clinical features of AUD. Second, CBD may influence AUD symptoms through its actions across the digestive, immune, and central nervous systems, collectively known as the microbiota–gut–brain axis (MGBA). Notably, emerging work suggests that alcohol and cannabinoids exert opposing effects on the MGBA. Alcohol is linked to immune dysfunction (e.g., chronic systemic inflammation in the brain and periphery) as well as disturbances in gut microbial species (microbiota) and increased intestinal permeability. These MGBA disruptions have been associated with AUD symptoms such as craving and impaired cognitive control. Conversely, existing preclinical data suggest that cannabinoids may confer beneficial effects on the gastrointestinal and immune system, such as reducing intestinal permeability, regulating gut bacteria, and reducing inflammation. Thus, cannabinoids may exert AUD harm‐reduction effects, at least in part, through their beneficial actions across the MGBA. This review will provide a brief introduction to the ECS and the MGBA, discuss the effects of cannabinoids (particularly CBD) and alcohol in the brain, gut, and immune system (i.e., across the MGBA), and put forth a theoretical framework to inform future research questions. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver disorders. Possible links have been recently found between the gut-microbiota and the host metabolism in development of NAFLD and obesity. Therefore, understanding the changes in intestinal microbiota during the progression of NAFLD, is important. In this study, the effect of Kombucha tea (KT), obtained by microbial fermentation of sugared black tea, was investigated on gut-microbiota during the progression of NAFLD. The results indicated a decrease in Erysipelotrichia class by treatment with KT in comparison to the methionine/choline-deficient (MCD)-fed db/db mice. Allobaculum, Turicibacter, and Clostridium genera, were only detected in MCD-fed db/db mice and were decreased after treatment with KT, whereas Lactobacillus was more abundant in MCD + KT-fed mice than in MCD only-fed mice and Mucispirillum, was found only in the MCD + KT-fed mice group. Our results demonstrated that the change of intestinal microbiota was influenced by KT intake, contributing to combat NAFLD. [ABSTRACT FROM AUTHOR]

Introduction: Worldwide, obesity poses a serious threat to public health and leads to higher costs and diseases. New research has shown that gut microbiota have a significant impact on how obesity and other metabolic problems are treated. Ginger is used as a spice and dietary supplement. It reduces inflammation and oxidative stress in the body and may have potential for treating obesity. The aim of the study was to investigate the beneficial effects of ginger in preventing obesity through the regulation of gut microbiota. Method: This review was conducted by searching databases including PubMed, Web of Science, Scopus, and Google Scholar. The keywords "obesity," "Gut-microbiota," and "Ginger" were examined without time limitation. English-language studies that investigated the Beneficial effects of ginger on prevention of obesity through modulation of gut microbiota met the study inclusion criteria. Findings: A total of 753 articles were obtained, out of which 14 related articles were entered for review. In 9 studies (64%), the beneficial role of ginger in preventing obesity through regulating gut microbes was mentioned. In 5 articles (35%), the direct effect of ginger in weight reduction and improvement of obesity-related diseases was also highlighted, and it was concluded the use of ginger supplement has a therapeutic effect. Conclusion: Although the impact of ginger on gut microbiota for preventing obesity still requires further investigation, the positive effects in the studied articles show incorporating ginger into weight loss and obesity treatment regimens can be beneficial. [ABSTRACT FROM AUTHOR]

In this study, male F344 rats were orally exposed to aflatoxin B1 (AFB1) at 0, 5, 25, and 75 μg/kg for 4 weeks. Rat feces were collected from 2 to 4 weeks following exposure and were assessed for gut-microbiota-dependent metabolites. Gut-microbiota-related organic acids were quantitated in the feces using 2-nitrophenylhydrazine derivatization coupled HPLC-profiling method which was validated and showed good reliability, accuracy and sensitivity. After 2-week exposure, AFB1 significantly reduced the levels of fecal short-chain fatty acids (SCFAs) with an over 70% reduction in the high-dose group (75 μg/kg). Mixed-effects model revealed an inverse correlation between AFB1 dose and fecal levels of SCFAs, but no significant time effect was found. When compared with the control, oral exposure to middle-dose AFB1 (25 μg/kg) resulted in remarkable elevations of fecal cholic acid (2.18-fold), linoleic acid (cis-9, cis-12–18:2) (11.3-fold), pentadecanoic acid (15: 0) (3.68-fold), pyruvic acid (4.56-fold), and 3-phenyllactic acid (3.74-fold), but deoxycholic acid level was reduced by 41% in the low-dose group (5 μg/kg). These results demonstrated the disruptions of several important gut-microbiota metabolic pathways, including the synthesis of SCFAs, pyruvic acid related pathways, metabolisms of amino acids, bile acids and long-chain fatty acids, which may further affect host digestive efficiency, energy supply, intestinal immunity, production of neurotransmitters, and enterohepatic cross-talk. Our study suggests that the impairment of gut-microbiota-dependent metabolism may contribute to pathological mechanisms of AFB1-induced adverse health effects. [ABSTRACT FROM AUTHOR]

Studies on termite symbiosis have revealed that significant symbiont lineages are maintained across generations. However, most studies have focused only on the worker caste. Little is known about the gut microbiota of reproductives, the most probable vectors for transmitting these lineages to offspring. Using 16S rRNA gene-based Illumina MiSeq sequencing, we compared the gut microbiota of swarming alates of the higher termite Nasutitermes arborum with those of their nestmates from the parental colony. The OTU-based alpha diversity indices showed that the gut microbiota of the alates was at least as diverse as those of non-reproductive adults. It was largely dominated by Spirochaetes mostly of the Treponema I cluster (63.1% of reads), the same dominant taxa found in soldiers and workers of this species and in workers of closely related Nasutitermes species. The termite-specific lineages also included other representative taxa such as several clusters of Bacteroidetes and Fibrobacteres-TG3 group. The microbiota of alates was dominated by a core set of host-specific lineages (87% of reads, 77.6% of OTUs), which were always present across all castes/stages. This first comprehensive survey of the microbiota of the founding reproductives of these xylophagous higher termites shows that the bulk of the host endogenous symbionts, mostly taxa that cannot thrive outside the gut, are brought from the parent colony. The royal pair therefore seems to be a key player in the transmission of symbionts across generations and thereby in host-symbiont codiversification. The high proportion of fiber-degrading lineages in their gut suggests a wood-rich diet unlike the larval stages. [ABSTRACT FROM AUTHOR]

Life on Earth harbours an unimaginable diversity of microbial communities. Among these, gut microbiome, the ecological communities of commensal, symbionts (bacteria and bacteriophages) are a unique assemblage of microbes. This microbial population of animal gut helps in performing organism's physiological processes to stay healthy and fit. The role of these microbial communities is immense. They continually maintain interrelation with the intestinal mucosa in a subtle equilibrium and help the gut for different functions ranging from metabolism to immunologic functions like upgradation of nutrient-poor diets, aid in digestion of recalcitrant food components, protection from pathogens, contribute to inter- and intra-specific communication, affecting the efficiency as disease vectors etc. The microbial diversity in the gut depends upon environmental competition between microbes, their sieving effects and subsequent elimination. Due to wide diversity of anatomy and physiology of the digestive tracts and food habits, the gut microbiome also differs broadly among animals. Stochastic factors through the history of colonization of the microbiome in a species and in situ evolution are likely to establish interspecies diversity. Moreover, the microbes offer enormous opportunity to discover novel species for therapeutic and/or biotechnological applications. In this manuscript, we review the available knowledge on gut microbiome, emphasising their role in health and health related applications in human. [ABSTRACT FROM AUTHOR]

Healthy interaction between microbes and the intestinal epithelium is essential for the normal development of the gut-immune system and overall health of the organism. [ABSTRACT FROM AUTHOR]

Fatalities from schistosome infections arise due to granulomatous, immune-mediated responses to eggs that become trapped in host tissues. Schistosome-specific immune responses are characterized by initial T helper type 1 ( Th1) responses and our previous studies demonstrated that myeloid differentiation primary response gene 88 (Myd88)-deficient mice failed to initiate such responses in vivo. Paradoxically, schistosomal antigens fail to stimulate innate cells to release proinflammatory cytokines in vitro. Since Schistosoma mansoni infection is an intestinal disease, we hypothesized that commensal bacteria could act as bystander activators of the intestinal innate immune system to instigate Th1 responses. Using a broad spectrum of orally administered antibiotics and anti-mycotics we analysed schistosome-infected mice that were simultaneously depleted of gut bacteria. After depletion there was significantly less inflammation in the intestine, which was accompanied by decreased intestinal granuloma development. In contrast, liver pathology remained unaltered. In addition, schistosome-specific immune responses were skewed and faecal egg excretion was diminished. This study demonstrates that host microbiota can act as a third partner in instigating helminth-specific immune responses. [ABSTRACT FROM AUTHOR]

The gut microbiota has been known to modulate the immune responses in chronic liver diseases. Recent evidence suggests that effects of dietary foods on health care and human diseases are related to both the immune reaction and the microbiome. The gut-microbiome and intestinal immune system play a central role in the control of bacterial translocation-induced liver disease. Dysbiosis, small intestinal bacterial overgrowth, translocation, endotoxemia, and the direct effects of metabolites are the main events in the gut-liver axis, and immune responses act on every pathways of chronic liver disease. Microbiome-derived metabolites or bacteria themselves regulate immune cell functions such as recognition or activation of receptors, the control of gene expression by epigenetic change, activation of immune cells, and the integration of cellular metabolism. Here, we reviewed recent reports about the immunologic role of gut microbiotas in liver disease, highlighting the role of diet in chronic liver disease. [ABSTRACT FROM AUTHOR]

Mucosal-associated invariant T (MAIT) cells are a subset of T lymphocytes expressing a semi-invariant T-cell receptor (TCR) present as TCR Vα7.2-Jα33 in humans and TCR Vα19-Jα33 in mice. They are activated by ligands produced during microbial biosynthesis of riboflavin that is presented by major histocompatibility complex class I-related (MR1) molecules on antigen-presenting cells. MAIT cells also possess interleukin (IL)-12 and IL-18 receptors and can be activated by the respective cytokines released from microbially stimulated antigen-presenting cells. Therefore, MAIT cells can be involved in bacterial and viral defenses and are a significant part of the human immune system. They are particularly abundant in the liver, an organ serving as the second firewall of gut microbes next to the intestinal barrier. Therefore, the immune functions of MAIT cells are greatly impacted by changes in the gut-microbiota and play important roles in the gut-liver pathogenesis axis. In this review, we discuss the nature and mechanisms of MAIT cell activation and their dynamics during different types of liver pathogenesis conditions. We also share our perspectives on important aspects that should be explored further to reveal the exact roles that MAIT cells play in liver pathogenesis in the context of the gut microbiota. [ABSTRACT FROM AUTHOR]

The gut–liver axis plays important roles in both the maintenance of a healthy liver and the pathogenesis of liver diseases, where the gut microbiota acts as a major determinant of this relationship. Gut bacteria-derived metabolites and cellular components are key molecules that affect the function of the liver and modulate the pathology of liver diseases. Accumulating evidence showed that gut microbiota produces a myriad of molecules, including lipopolysaccharide, lipoteichoic acid, peptidoglycan, and DNA, as well as short-chain fatty acids, bile acids, trimethylamine, and indole derivatives. The translocation of these components to the liver exerts beneficial or pathogenic effects by interacting with liver immune cells. This is a bidirectional relationship. Therefore, the existence of crosstalk between the gut and liver and its implications on host health and diseases are essential for the etiology and treatment of diseases. Several mechanisms have been proposed for the pathogenesis of liver diseases, but still, the mechanisms behind the pathogenic role of gut-derived components on liver pathogenesis remain elusive and not understandable. This review discusses the current progress on the gut microbiota and its components in terms of the progression of liver diseases, and in turn, how liver diseases indirectly affect the intestinal function and induce intestinal inflammation. Moreover, this paper highlights the current therapeutic and preventive strategies used to restore the gut microbiota composition and improve host health. [ABSTRACT FROM AUTHOR]

Chicken gastrointestinal tract is an important site of immune cell development that not only regulates gut microbiota but also maintains extra-intestinal immunity. Recent studies have emphasized the important roles of gut microbiota in shaping immunity against viral diseases in chicken. Microbial diversity and its integrity are the key elements for deriving immunity against invading viral pathogens. Commensal bacteria provide protection against pathogens through direct competition and by the production of antibodies and activation of different cytokines to modulate innate and adaptive immune responses. There are few economically important viral diseases of chicken that perturb the intestinal microbiota diversity. Disruption of microbial homeostasis (dysbiosis) associates with a variety of pathological states, which facilitate the establishment of acute viral infections in chickens. In this review, we summarize the calibrated interactions among the microbiota mediated immune modulation through the production of different interferons (IFNs) ILs, and virus-specific IgA and IgG, and their impact on the severity of viral infections in chickens. Here, it also shows that acute viral infection diminishes commensal bacteria such as Lactobacillus, Bifidobacterium, Firmicutes, and Blautia spp. populations and enhances the colonization of pathobionts, including E. coli, Shigella, and Clostridial spp., in infected chickens. [ABSTRACT FROM AUTHOR]

The study evaluated the symptoms, acceptance, and digestibility of bread made from transgenic low-gliadin wheat, in comparison with gluten free bread, in Non-coeliac gluten sensitivity (NCGS) patients, considering clinical/sensory parameters and gut microbiota composition. This study was performed in two phases of seven days each, comprising a basal phase with gluten free bread and an E82 phase with low-gliadin bread. Gastrointestinal clinical symptoms were evaluated using the Gastrointestinal Symptom Rating Scale (GSRS) questionnaire, and stool samples were collected for gluten immunogenic peptides (GIP) determination and the extraction of gut microbial DNA. For the basal and E82 phases, seven and five patients, respectively, showed undetectable GIPs content. The bacterial 16S rRNA gene V1-V2 hypervariable regions were sequenced using the Illumina MiSeq platform and downstream analysis was done using a Quantitative Insights into Microbial Ecology (QIIME) pipeline. No significant differences in the GSRS questionnaires were observed between the two phases. However, we observed a significantly lower abundance of some gut genera Oscillospira, Dorea, Blautia, Bacteroides, Coprococcus, and Collinsella, and a significantly higher abundance of Roseburia and Faecalibacterium genera during the E82 phase compared with the basal phase. The consumption of low-gliadin bread E82 by NCGS subjects induced potentially positive changes in the gut microbiota composition, increasing the butyrate-producing bacteria and favoring a microbial profile that is suggested to have a key role in the maintenance or improvement of gut permeability. [ABSTRACT FROM AUTHOR]