What Is Microbiota

C O N T E N T S:


  • During the past decade a large number of genomic studies have reported associations between our gut microbiota composition and metabolic disorders.(More…)
  • The first theme is that the microbiota of the human gut responds rapidly to large changes in diet.(More…)
  • Lam YY, Ha CW, Campbell CR et al (2012) Increased gut permeability and microbiota change associate with mesenteric fat inflammation and metabolic dysfunction in diet-induced obese mice.(More…)


What Is Microbiota
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During the past decade a large number of genomic studies have reported associations between our gut microbiota composition and metabolic disorders. [1] To understand how antibiotic effects on bacterial populations could lead to shifts in gut redox potential, we investigated the dynamics and metabolism of microbiota across treatment in mice. [2] Beyond identifying a role for microbiota in shaping gut redox potentials, our results more broadly illustrate how microbial factors can be important in addition to host factors for determining abiotic conditions in the gut through the balancing of production and consumption of resources. [2] Thank you for submitting your article “Antibiotic induced changes in the microbiota disrupt redox dynamics in the gut” for consideration by eLife. [2] Increasing amounts of evidence now point to the importance of the collections of bacteria found in our guts — often known as the “gut microbiota” — in various aspects of our well-being. [3] Unlike nitrate and oxygen, though, much of the fumarate in the gut is likely produced by the microbiota itself ( Fischbach and Sonnenburg, 2011 ; El Aidy et al., 2013 ). [2] Collectively, the diverse range of microorganisms coexists and builds cooperative ecological community referred to as microbiota. 1 The GI tract has an abundance of microorganisms that is termed “gut microbiota?. [4]

This is known in many contexts and should be rephrased to something about a generalized function of antibiotics or implications for understanding and controlling the human microbiota and disease. [2] Changes in redox potential under antibiotics would in turn be expected to yield insight into the forces structuring the composition and function of the microbiota. [2] Elevated redox potential due to a host immune response could restrict the microbiota beyond direct antibiotic mortality as inflammation would introduce additional oxidative stress into microbial ecosystems. [2] Notably, our data suggest that ones produced by the microbiota rather than the host, like fumarate, were less available under antibiotic pressure. [2]

Microbial communities (microbiota) influence human and animal disease and immunity, geochemical nutrient cycling and plant productivity. [5] We next investigated if abiotic recovery led to compositional recovery or if dispersal ( i.e., migration of microbes) from unimpacted microbial populations was necessary for microbiota to exhibit resilience and return to a pre-treatment state. [2]

Specifically, mice housed in static cages with aspen bedding had a clearly different cecal microbiota composition compared to all other groups. [6] When the microbiota composition from these different sections was analyzed, it was revealed that caging and bedding type had a highly significant effect on the cecal microbiota. [6]

In the first part of the Microbiota & Food 2018, we will discuss the recent advances in microbiota and food utilization, its characterization, its role and its clinical impact on health. [7] The International Society of Microbiota (ISM) organizes the first ISM Symposium on Microbiota & Food, which will be. [8] The aim of Microbiota & Food 2018 is to provide some ideas and strategies to help integrate an understanding of the industry perspective with the clinical and scientific perspectives to initiate these projects. [8] The committee will also highlight the toxicity aspects of food processing and exposure to various external component or unidentified contaminants and the impact on the microbiota after ingestion and exposure. [7]

The infant skin microbiota may serve as a reservoir of bacteria that contribute to neonatal infections and stimulate local and systemic immune development. [5] The microbiota only returned to its previous state when the treated mice were housed together with non-treated mice. [2] The microbiota can differ even in mice from the same vendor, especially if mice are housed in different rooms/facilities. [2] The authors should clarify whether the mouse microbiota was similar in mice ordered at different times. [2] It was found that all mice shared a comparable baseline microbiota. [6] This was expected because mice that live together commonly exchange microbes, for instance by eating each other’s feces, and the treated mice received new species to replenish their microbiota. [2] This suggested that despite coming from the same vendor, our mice indeed had different microbiota. [2] Male C57BL/6 mice (Charles River Laboratories, Wilmington MA) 8-10 weeks of age with a native microbiota were used for all experiments. [2]

Prof. Desiderio Passali, from University of Siena, Italy will present his studies on the “Role of nasal Microbiota in respira. [8] The role of the oral microbiota in HIV-infected youth is not known. [5] It is not clear why this happened, but the authors hypothesize that unknown volatile or aromatic compounds, e.g. urinary ammonia, could play a role in shaping of the microbiota. [6]

This result corroborates our model that members of the Enterobacteriaceae use respiration to bloom under disturbed conditions, and it highlights the potential for manipulating electron acceptor availability or usability to engineer the microbiota. [2] Dr. Sara Federici from Weizmann Institute of Science, Israel will join the Porto Microbiota 2018 Congress which will be held. [8] Paul Forsythe from McMaster University, Canada will join the Porto Microbiota 2018 Congress which will be held in Octobe. [8] Dr Marcin Ufnal from Medical University of Warsaw, Poland will join the Porto Microbiota 2018 Congress which will be held in. [8]

For this 5th edition of ISM World Congress on Microbiota, which was held on October 26-27, 2017, the organizing committee h. [8] The scientific and organizing committee of the International Society of Microbiota informed you that the 6th World Congr. [8] The International Society of Microbiota is honored to welcoming attendees coming from all around the world, from academics an. [8] Copyright International Society of Microbiota – All right reserved. [8]

Adoption of thermal processing of the diet drives human evolution and gut microbiota diversity changes in a dietary habit-dependent manner. [5] More dramatic diet regimes, such as Western diet and synthetic diets, are known to elicit significant changes in the gut microbiota. [6] The biologists identified the precise order of organic molecules known as nucleotides from the DNA of gut microbiota to determine which bacteria were present and at what levels after the diet was administered. [9] A myriad of factors can influence the gut microbiota composition of laboratory rats and mice: diet, stress, circadian rhythm, vendor source, how they are housed, and more. [6] A successional return to conventional community composition only occurred, though, when mice were co-housed and shared gut microbiota, indicating that microbial dispersal is necessary above and beyond environmental recovery for the return of normal microbiota community structure. [2] To test if inhibition of bacterial populations by antibiotics could directly contribute to redox potential dynamics, we used an ex vivo human gut system based on a continuous-flow bioreactor ( McDonald et al., 2013 ), which allowed the propagation of a stable microbial community representative of the human gut microbiota with all major phyla represented ( Figure 2–figure supplement 1 ). [2] “As bacterial competition for electron acceptors can be a key ecological factor structuring microbial communities, these results support the potential for manipulating gut microbiota through managing bacterial respiration.” [2] In return, it assists the body in the digestion of complex carbohydrates, produces vitamins (e.g. vitamin B12), generates non-nutrient essential factors, regulates the maturation of the immune cells, and prevents the colonisation of harmful microorganisms. 4 As such, the equilibrium of gut microbiota is essential to maintain good health. [4] Dec. 19, 2017 – Our gut hosts a community of trillions of microbes, called the gut microbiota, and we are becoming increasingly aware that this has significant effects on many aspects of our health. [9] The murine study published in Science focused on the effects of antibiotics and gut microbiota in the presence of liver tumors. [10] The study, published today in the journal Cell, is the first to establish a causal link between seizure susceptibility and the gut microbiota — the 100 trillion or so bacteria and other microbes that reside in the human body’s intestines. [9] First study author Jonas Zierer also explains that understanding which factors are likely to alter the activity of our gut microbiota is of great help in the quest when it comes to developing better therapies to prevent conditions such as obesity and diabetes. [3] There are only a few studies on how different cage types, bedding materials, and chow diets affect the gut microbiota, such as this new study out of University of Missouri. [6] Maintain a healthy lifestyle and diet is also important for a healthy gut microbiota. [4] A healthy diet goes a long way to protect the balance of gut microbiota. [4] “This suggests that the gut microbiota is required for the diet to effectively reduce seizures.” [9]

In recent years, human microbiota, especially gut microbiota, have emerged as an important yet complex trait influencing human metabolism, immunology, and diseases. [5] To fit with this extraordinary revolution, the agro-food industries have to prepare and initiate new ideas and new products for which the formulation will have a positive impact on human gut microbiota and by consequence on human health. [8] Thursby E, Juge N. Introduction to the human gut microbiota. [4] The gut microbiome, or gut microbiota, describes the diverse environment of microorganisms in the human and animal digestive tract. [10] Gut microbiota were cultured from human stool in a flow-through bioreactor system (Infors, Bottmingen Switzerland) following previous work ( McDonald et al., 2013 ). [2]

Imbalances of gut microbiota composition are linked to a range of metabolic perturbations. [5] Avoid smoking – Smoking is found to alter both the composition of the gut microbiota as well as decrease its diversity. [4] Studies have shown that alteration of the composition of the gut microbiota influences the incidence and progression of colorectal cancer. [4] Fecal pellets were collected one week after arrival, and the fecal gut microbiota composition was analyzed in all the groups. [6]

The gut microbiota is closely associated with gastrointestinal (GI) motility disorder, but the mechanism(s) by which bacteria interact with and affect host GI motility remains unclear. [5] Oct. 20, 2016 – Our intestine hosts a complex ecosystem of bacteria; we call it the gut microbiota, which includes at least 1000 difference species. [9] The early-life gut microbiota plays a critical role in host metabolism in later life. [5] We know that our gut microbiota play a crucial role in regulating our overall health, particularly our fat stores. [3] We have now tempered the language in the abstract and refocused the final sentence for implications for understanding the relationship between the gut microbiota and health. [2] By eradicating H. pylori, a person will tend to overeat and increase the risk of obesity. 6 Hence, gut microbiota equilibrium is the key to health. [4]

This is an important question given the variation in gut microbiota known to exist between mice both within and between vendors (Rosshart et al. 2017, Rausch et al. 2016, Ivanov et al. 2009, Campbell et al. 2012). [2] The obvious advantage of fecal pellet sampling is ease of longitudinal gut microbiota surveys, but including groups of mice to be euthanized in intervals would also support analysis of the cecal microbiota. [6]

Together, our findings suggest new ecological models for how antibiotics reshape the gut microbiota and for how redox shifts could be associated with enteric disease. [2] Reese et al. have now investigated what happens to the gut environment after antibiotic treatment and how the gut microbiota recovers. [2]

The gut is home to a large and diverse community of bacteria and other microbes, known as the gut microbiota. [2] Mar. 6, 2014 – Our intestines harbor an astronomical number of bacteria, around 100 times the number of cells in our body, known as the gut microbiota. [9] Several by-products of the gut microbiota, such as the short-chain fatty acids, are known to be able to destroy cancer cells or suppress cancer growth. [4]

Variation in induced models of autoimmunity has been attributed to the housing environment and its effect on the gut microbiota. [5] While individual electron acceptors are sometimes considered in studies of the gut microbiota, they are rarely presented in concert nor is overall redox potential measured. [2] Redox potential, a metric of the environmental capacity for reducing chemical reactions ( i.e., those involving the gain of electrons) to occur, is a composite measurement of various factors that influence gut microbiota structure ( Cowley et al., 2015 ; Friedman et al., 2017 ; Dhall et al., 2014 ). [2]

It is widely accepted that there are hundreds of different species of bacteria that can make up an individual’s gut microbiota; in fact, at least a third are shared amongst a majority of people with the other two thirds being unique to each individual. [10] In the present study, we examined the gut microbiota of women with gestational diabetes mellitus (GDM) and normoglycae. [5] A healthy and thriving gut microbiota can protect us from cancer. [4] Fibres – Fibres are non-digestible carbohydrates which serve as fuels, or pre-biotics, to the gut microbiota. [4] Identifying how these drivers interact is necessary both for a more complete understanding of the gut microbiota and for developing rational interventions. [2]

Interestingly, the different diets had very little effect on the intestinal microbiota. [6] The sunny city of Porto will host the 6th World Congress on Targeting Microbiota in October 28-30, 2018. [8] The abstracts book of the 5th World Congress on Targeting Microbiota, which will be held in Berlin, Germany on October 26-27. [8] The scientific committee of the 5th World Congress on Targeting Microbiota discerned the ISM oral communication award to Dr. [8] The scientific committee of the 5th World Congress on Targeting Microbiota 2017 published the list of short presentations a. [8] Dr. Markus Egert from Furtwangen University, Germany will give a talk during the 5th Targeting Microbiota World Congress. [8] During two days, more than 70 posters were presented during Targeting Microbiota Congress. [8]

The first theme is that the microbiota of the human gut responds rapidly to large changes in diet. [11] The microbial colonization of the human gut begins at birth and immediately thereafter; but some recent studies reporting the presence of bacteria in placenta, amniotic cavity, umbilical cord, and meconium have suggested that the dynamic and complex process of infant microbiota colonization may have already started in-utero. [12] These results are consistent with the fact that the fermentation of dietary fibre represents one of the dominant microbial metabolic activities in the colon, the region of the gut in which the microbiota is most dense 35, 36. [11] Changes in the microbiota can result in a “leaky gut” that permits the exit of microorganisms and compounds that are a result of their metabolism (metabolites) into our bodies? circulation. [13] The human gut is a bioreactor with a microbiota that typically encompasses hundreds or thousands of bacterial taxa, which predominantly belong to two phyla: Firmicutes and Bacteroidetes 2 – 5. [11] Gut brain axis: Diet microbiota interactions and implications for modulation of anxiety and depression. [12] This might be attributed to altered microbiota equilibrium i.e. the reduced levels of beneficial/commensals and elevated levels of opportunistic pathobionts and also the consequent altered array of microbial metabolites around the gut lining ( Fig. 4 ). [12] It can be speculated that the gut epithelium that acts as a barrier between gut microbes and systemic circulation, might be playing a role in the association of microbiota and inflammaging. [12] Gut instincts: Microbiota as a key regulator of brain development, ageing and neurodegeneration. [12] Dynamics of the gut Bifidobacterium microbiota during the first three years of life: A quantitative assessment. [12] Microbiota controls the homeostasis of glial cells in the gut lamina propria. [12]

These data indicate that the extent of the diversity might be an important factor for metabolic health, which is consistent with findings from microbiota studies that have focused on traditional human societies. [11] Three metagenomic studies 13, 21, 51 have shown that improved metabolic health is associated with a relatively high microbiota gene content and with an increased microbial diversity. [11] Several studies in humans indicate that there is a population-specific ‘ceiling’ on microbiota diversity and metabolic output. [11] Human intervention studies from the past decade have revealed the extent to which different aspects of the microbiota can be influenced through dietary change; this can be summarized by three main themes. [11] Because dietary change often involves both the elimination and addition (that is, the substitution) of dietary components, even the most successful intervention studies can raise questions about which diet modification was responsible for the change in the microbiota. [11]

Changes in the rumen epithelial microbiota of cattle and host gene expression in response to alterations in dietary carbohydrate composition. [14] The existence of these fast, diet-induced dynamics is supported by evidence from people who switch between plant- and meat-based diets, who add more than 30 grams per day of specific dietary fibres to their diet or who follow either a high-fibre–low-fat diet or a low-fibre–high-fat diet for 10 days; in all cases, the composition and function of the microbiota shifted over 1–2 days 18, 20, 23. [11] The influence of diet on aspects of microbiota function might also help to explain how a specific metabolic input can alter microbiota composition over time. [11] Diet and, in particular, polysaccharides serve as primary modulators of the composition and function of the microbiota. [11] If the fibre composition of the diet is matched to the needs of a low-diversity microbiota (bottom right) by limiting the types of complex carbohydrate that are available, the levels of production of certain short-chain fatty acids, such as propionate, might increase. [11] A switch to a diet rich in saturated fatty acids shifts the composition of the microbiota 44. [11] A diet high in resistant starch modulates microbiota composition, SCFA concentrations, and gene expression in pig intestine. [12]

In a multigenerational study in mice, the consumption of a Western-style diet exacerbated the loss of microbiota diversity compared with a diet that was rich in microbiota-accessible carbohydrates, and the extinction of taxa corresponded with a predicted loss in diversity of glycoside hydrolases 63. [11] In a study that focused on the enzymatic activity of trimethylamine lyase, mice that harbour microbiotas with low production of trimethylamine (TMA) could be converted into high producers when their diet was supplemented with the TMA-containing compound L-carnitine for 10 weeks 27. [11] The effects were reversed when reverting the KD microbiota to those that would normally be found in CD mice, “suggesting that persistent interactions between the KD microbiota, diet, and neuronal activity are required,” the authors point out. [15] Importantly, the lean microbiota could only invade and prevent increased adiposity when the recipient mice consumed a diet that was low in fat and high in fruits and vegetables. [11] Certain recurrent physiological states in mammals, such as the non-hibernating period in bears 41 and advanced pregnancy 42, result in a markedly altered microbiota with an increased capacity to harvest energy from the diet without metabolic derangement. [11] The altered microbiota that is observed in genetically obese mice 11, 12 is sufficient to promote increased adiposity in lean mice that receive a microbiota transplant 12, demonstrating that the microbiota contributes to the regulation of adiposity. [11] A model of adipose inflammation that is dependent on the microbiota but independent of diet is supported by evidence from Swiss Webster mice. [11] Consistent with the idea that the microbiota reinforces the diet, supplementation with Prevotella produces an improved tolerance to glucose only when mice are fed a standard diet that is rich in fibre, and not a Western-style diet, which is devoid of fibre 22. [11] Changes in the diet might be more important for reaping the health benefits that the microbiota can provide. [11] The Mediterranean Diet has been shown to reduce the risk for Alzheimer’s disease, and the health of our microbiota may be one of the reasons why this diet is so beneficial. [13] Bile acids, formed by the microbiota from host cholesterol, are another group of metabolites with a profound effect on human health 82. [11] Prebiotic fiber, although indigestible by a human, is a source of food for the microbiota that promotes the growth of healthful microorganisms such as bifidobacterial and lactic acid bacteria. [13] Despite efforts, there are no reports on the role of segmented filamentous bacteria in people, but other bacteria in the human microbiota might have developed similar functions. [11] Intriguingly, this pro-longevity effect has been found to be indirectly mediated by its influence on bacteria, specifically involving the suppression of bacterial folate metabolism, thereby highlighting the importance of exploring the possible pro-longevity effect of such drugs and also elucidating how microbiota and microbial-metabolites play a role in antiaging effects. [12] These findings suggest that simple carbohydrates and fats could exert unexpected effects on the host metabolism through the microbiota. [11] It is reasonable to hypothesize that the enteric nervous system undergoes some degenerative changes in line with the changes in the host physiology, metabolism, microbiota and immune system during aging ( Fig. 4 ). [12] TGR5 and FXR both have a major impact on host metabolism 84 and, accordingly, an altered microbiota might affect host physiology by modulating the signals that pass through these receptors. [11] Bariatric surgery is associated with an altered microbiota and metabolism of bile acids 16, 90. [11] Notably, high diversity in the microbiota corresponds with high levels of short-chain fatty acid production in rural farmers in Burkina Faso 19, as well as with the enrichment of genes in the microbiome of hunter–gatherers that are associated with the metabolism of complex carbohydrates 62. [11] Following a vegan diet for at least 6 months or a high-fibre–low-fat diet for 10 days were insufficient to substantially increase microbiota diversity or production of faecal short-chain fatty acids 28. [11] When the diversity of the microbiota is high and the diet contains many types of complex carbohydrates (top right), a relatively high percentage of complex carbohydrates will be accessible to the microbiota. [11] This indicates that the microbiota might need to already have the capacity to degrade certain complex carbohydrates in the diet to reap the potential benefits of microbiota-accessible carbohydrates. [11] The complex carbohydrates that are associated with whole grains and that were metabolically accessible to the microbiotas of the responders might therefore have been inaccessible to non-responders who also did not routinely consume high-fibre diets. [11] The data suggest strong alterations of the ruminal epimural microbiota in response to changes in the nutritive patterns of the diet. [14] One theory is that the microbiota of industrialized nations are experiencing a widespread change in functional capacity (for instance, altered production of short-chain fatty acids), which is contributing to modern health issues such as obesity 56 – 58. [11] The enteric nervous system promotes intestinal health by constraining microbiota composition. [12] Some, but not all, cross-sectional studies reported that long-term dietary trends are linked to features of microbiota composition 20, 25, 27, 28. [11] Excessive intake of artificial sweeteners and frequent use of antibiotics are two other factors that affect the composition of our microbiota. [13] This interesting thesis highlights several factors acknowledged for their influence on microbiota development, such as antibiotics, delivery mode and feeding strategy, as well as a potential influence of gender, respiratory support and maternal preeclampsia. [16] They are frequently exposed to interventions during hospitalisation, such as caesarean section delivery, antibiotics and respiratory support, which likely affect the development of their microbiota. [16] The thesis describes that antibiotic treatment during the first week of life impacts microbiota development, particularly by increasing Enterococcus species, while decreasing beneficial Bifidobacterium species. [16] The impact of antibiotics on microbiota development in late preterm infants was investigated. [16]

Emulsifiers and artificial sweeteners have been shown to be involved in the development of metabolic syndrome features through their modulation of the microbiota in mice 46, 47. [11] Another approach is to transfer microbiotas from humans to mice, and this is particularly powerful when focused on twin cohorts to control for human genetics 14, 15, 51. [11] To improve the understanding of how the microbiota affects the metabolism in humans, metagenomics, transcriptomics, proteomics and metabolomics data from key target tissues and the microbiota during various disease states and interventions should be combined to provide a map of co-occurrences. [11] Notably, individuals whose microbiota and glucose tolerance respond to a whole-grain intervention tend to consume diets that are higher in fibre. [11] This study showed that a microbiota from a lean individual could invade the microbiota of an obese individual and provide protection from weight gain, but that the invasion and protection was dependent on diet. [11] In a separate study, bacterial representatives from the microbiota of lean individuals were associated with an increased production of short-chain fatty acids, whereas the microbiota of obese individuals had an increased abundance of genes that are involved in biosynthesis of branched-chain amino acids, which are associated with impaired sensitivity to insulin 14. [11] The amount of fibre that can be metabolized (for example, through the enzymatic degradation of glycosidic linkages and the fermentation of liberated monosaccharides into short-chain fatty acids) will depend on many factors, including the composition of the microbiota. [11] The ability to easily access and reprogramme the composition and function of the microbiota make it an attractive target for intervention. [11] Despite detectable responses of the microbiota within 24 hours of dietary intervention, a 10-day feeding study in 10 people 20 failed to alter the major compositional features and the overall classification of each participant’s microbiota. [11] A dietary intervention that includes a boosted intake of fibre and a decreased intake of energy can increase microbiota diversity — as defined by the gene content of the faecal metagenome — for individuals who start with a low microbiota gene content, but not those who start with a high gene content 21. [11] Data-processing algorithms, such as machine learning, can be used to identify aspects of the clinical profile of individuals (including data on the microbiota) that help to predict the response of others to dietary interventions. [11] The inclusion of high-quality hay (HQH), in place of concentrates, shifts dietary carbohydrate intake, and the extent to which these shifts effect epimural microbiota and epithelial gene expression of the rumen has not yet been evaluated. [14] Mice that consume lard and receive the microbiota of those fed fish oil are protected against obesity 44, which demonstrates that the modified microbiotas themselves have a protective effect. [11] The microbiota of mice suppress the expression of intestinal angiopoietin-like protein 4, an inhibitor of the enzyme lipoprotein lipase, which increases lipoprotein-lipase activity in adipose tissue and promotes the storage of fat 7. [11] The intestinal metabolome: An intersection between microbiota and host. [12] Hay is believed to be healthier and more ecological sustainable for cattle than are concentrates, although the effects of feeding hay with enhanced sugar and protein content on epimural microbiota and host gene expression have not yet been evaluated. [14] The effect of microbiota and the immune system on the development and organization of the enteric nervous system. [12] A healthy GI and microbiota development and function during early life coincides with the development and function of the immune system. [16] June 11 2018, Romy D. Zwittink will publicly defend her PhD thesis highlighting the gastrointestinal function and microbiota development in preterm infants during early life. [16] Development of the human gastrointestinal microbiota and insights from high-throughput sequencing. [12] Walker AW, et al. Dominant and diet-responsive groups of bacteria within the human colonic microbiota. [11] Dietary modulation of the human colonic microbiota: Introducing the concept of prebiotics. [12] The source of dietary fat might therefore have specific interactions with the microbiota that lead to altered interactions with the innate immune system and contribute to metabolic diseases. [11] The absence of dietary fibre together with an abundance of nutrients that negatively affect the microbiota could be of considerable importance for understanding metabolic diseases. [11]

Notably, an important and unwavering commonality of Western dietary trends is the paucity of plant-based dietary fibre 48, an important fuel for the microbiota. [11] How can we use what scientists have learned about the microbiota to reduce our risk of Alzheimer’s disease? One important message is that our microbial inhabitants need us to feed them properly. [13] Feed your microbiota lots of fiber, fruit, and vegetables! This is one of the ways in which you can improve your health, reduce systemic inflammation, and even, perhaps, reduce your risk for Alzheimer’s disease. [13] Our microbiota undergoes the most prominent deviations during infancy and old age and, interestingly, our immune health is also in its weakest and most unstable state during these two critical stages of life, indicating that our microbiota and health develop and age hand-in-hand. [12] Bifidobacterium microbiota and parameters of immune function in elderly subjects. [12] The diversity of the microbiota will probably remain low and it might not be able to provide as many functions as a diverse microbiota. [11] Overall, these data suggest that the production of short-chain fatty acids is affected by the existing diversity within a microbiota. [11]

Beginning in 2001, scientists observed that mice with different microbiota had different biologies, suggesting that resident bacteria could modulate the host’s gene expression. [17] When the mice are fed a peanut-based, ‘ready-to-use’ therapeutic food, their weight transiently increases and their microbiota normalize 115. [11] These data provide evidence that artificial food additives might contribute to metabolic disease through disruption of the microbiota. [11]

Carbohydrates that can be metabolized by the microbiota are known as microbiota-accessible carbohydrates 61 and can be contrasted with those that pass through the digestive tract without undergoing metabolic transformation. [11] When fed high levels of resistant starch, individuals who fail to show a bloom in Ruminococcus bromii and its relatives also have the highest levels of undigested starch in their stool, which supports the idea that the composition of the microbiota determines whether a carbohydrate is accessible to the microbiota 23. [11]

TMA production serves as an excellent example of the interaction between the diet and the microbiota. [11] Microbiotas that are capable of producing TMA make the metabolite only when compounds that contain trimethyl ammonium are present in the diet, and some microbiotas (such as those of vegans) are poor producers of TMA 27, even when precursor compounds are transiently provided through the diet. [11]

A randomised crossover study investigating the effects of galactooligosaccharides on the faecal microbiota in men and women over 50 years of age. [12] At least some of this effect is mediated by an altered microbiota 89. [11]

The gut-brain-axis (GBA) is a bidirectional communication system between the gastrointestinal tract microbiota and the brain including various metabolic, immunological, endocrine, and neuronal signals derived from individual bacterial cells and their metabolites. [18] Sensitive quantitative analysis of the meconium bacterial microbiota in healthy term infants born vaginally or by cesarean section. [12] Srinivasan S, et al. Bacterial communities in women with bacterial vaginosis: high resolution phylogenetic analyses reveal relationships of microbiota to clinical criteria. [11]

It will also be important to gain a more nuanced understanding of the foundational principles of the microbiota, such as the cross-sectional or longitudinal spatial organization of interactions between the host and its microbes in the intestine 118. [11] It is therefore important to understand how the preterm infant gastrointestinal tract is functioning, which bacteria colonise, what the bacteria are doing and how microbiota establishment is affected. [16] Experiments could be performed using specific bacteria from lean microbiotas with the aim of developing next-generation probiotics. [11]

Donia MS, Fischbach MA. Small molecules from the human microbiota. [11] Kettle H, Louis P, Holtrop G, Duncan SH, Flint HJ. Modelling the emergent dynamics and major metabolites of the human colonic microbiota. [11]

A new science of the microbiome–meaning, simply, the microorganisms in an environment–emphasizes that all plants and animals on Earth evolved in combination with microorganisms and asks how microbiota interact with their hosts. [17] The longer the treatment with antibiotics, the longer the disturbance of the microbiota. [16] The capacity to metabolize tauro-β-muricholic acid, a naturally occurring FXR antagonist 86, 87, is essential for the microbiota to induce obesity and steatosis, as well as impaired tolerance to glucose and insulin 87 – 89. [11] They are metabolized by the microbiota in the lower part of the small intestine and the colon to generate secondary bile acids 83. [11] It could miss information on how the microbiota affects nutrient absorption in the small intestine through its impact on glucose transporters and bile acids, which are essential for the absorption of lipids and fat-soluble vitamins. [11]

Your microbiota are mostly harmless, but many are functionally important to you also, crowding out more harmful microbes, teaching your immune system to recognize enemies, and influencing behavior like your appetite. [17] Owing to the complexity and individuality of each microbiota, the rate at which this potential can be realized is unknown. [11] Schwiertz A, et al. Microbiota and SCFA in lean and overweight healthy subjects. [11] Hsiao EY, et al. Microbiota modulate behavioral and physiological abnormalities associated with neurodevelopmental disorders. [11] The microbiota produces a vast number of metabolites and much work remains to be done to investigate fully their functions in physiology and pathophysiology. [11] The measurement of multiple aspects of individuality, including the microbiota, will provide insight into the characteristics of people who respond beneficially to a given intervention and will pave the way for microbiota-focused precision nutrition. [11] In any case, it is well acknowledged that the foundational microbiota configuration keeps on fluctuating markedly during infancy, especially during the first three years, until finally settling into a somewhat stable structure resembling that of adult-microbiota. [12] First implementation of frozen, capsulized faecal microbiota transplantation for recurrent Clostridium difficile infection into clinical practice in Europe. [12]

It has also been known that hosts with perturbed intestinal motility can develop gut microbial dysbiosis and intestinal pathology, clearly hinting towards a profound role for the ENS in constraining gut microbiota composition and preventing the overgrowth of bacterial lineages that could otherwise drive diseases. [12] The gut microbiota plays a central role in various host physiological functions including degradation of fibrous foods, energy supply and harvest, lipid storage and metabolism, synthesis of vitamins, suppression of harmful bacteria and maintenance of intestinal barrier integrity. [12] Given that the gut microbiota has a strong impact on numerous aspects of host health and that the aberrations in the microbiota diversity and functionality are associated with various inflammatory conditions, it appears plausible to look at the human biology from a microbiota perspective as well and to envisage certain microbiota deviations as hallmarks of agingprocess. [12] Strategies for modulating the gut microbiota to improve human health a, The collection and comparison of multi-omics data from healthy people and those who are affected by metabolic disorders will implicate various genes, pathways and molecules as potential targets for intervention. [11] To accomplish this, we have ontologically divided the review into: (a) a brief outline of the gut microbiota development; (b) an overview of age-induced changes in the microbiota; (c) a discussion of potential implication of microbiota changes in the senescence of immune and inflammatory health; and (d) an outline of potential microbiota-targeted therapies for amelioration of human aging. [12] Controlled dietary interventions that document the utility of various supplements, probiotics, nutrients and foods in modulating aspects of the gut microbiota and human health are required. [11] In line with probiotics, many prebiotics have also been explored in human studies, mainly in context to their positive effects on the modification of human gut microbiota, i.e. promoting beneficial microbes and suppressing harmful bugs. [12] Effect of prebiotics on the human gut microbiota of elderly persons. [12] Experimental models that lack a gut microbiota offer further power for determining whether the effects of diet in the host depend on the microbiota. [11] The gut microbiota represents a key intermediary between diet and host physiology and plays a role in modulating metabolic, neurological, and metabolic pathways that might be relevant to KD diet-induced seizure protection, they suggest. [15] The metabolic role of gut microbiota in the development of nonalcoholic fatty liver disease and cardiovascular disease. [12] Gut microbiota in health and disease: An overview focused on metabolic inflammation. [12] While these deviations are largely natural, inevitable and benign, recent studies show that unsolicited perturbations in gut microbiota configuration could have strong impact on several features of host health and disease. [12] We finally conclude with a discussion of the prospective implications of this age-associated alternations in the gut microbiota, with specific regard to ameliorating the senescence and postponing the ill-health of old-age in order to improve the human health and disease in old-age. [12] The gut microbiota provides a powerful route to influencing human health. [11] Gut microbiota composition correlates with diet and health in the elderly. [12] A plant-based diet could significantly alter the composition of the gut microbiota, although a change in diversity was not observed 18. [11] The third theme is that a particular change in diet can have a highly variable effect on different people owing to the individualized nature of their gut microbiota. [11] Changes in the gut microbiota of aging individuals has a high inter-individual variability due to disease manifestation, medication, diet, and environmental exposure. [18] Consumption of a complex diet (top right) might result in increased levels of production of multiple types of short-chain fatty acids and helps to recruit additional diversity to the gut microbiota. [11] Interactions between the diet and the gut microbiota dictate the production of short-chain fatty acids Dietary fibre is a source of complex carbohydrates, which are required for the production of short-chain fatty acids such as acetate, butyrate and propionate. [11] These differences begin to diminish and the overall gut microbiota composition starts getting relatively stable at weaning i.e. after introducing solid foods in babies? diet. [12] “Probiotics dramatically change the architecture of the gut microbiota, not only in its composition but also in respect to how the foods that we eat are metabolized. [18] Intriguingly, it has also been demonstrated that the ENS maintains and promotes intestinal health via modulating the gut microbiota community composition and that the microbiota composition would become altered or abnormal without a functional ENS. [12] It is found that elder people have a different gut microbiota profile compared to healthy adults, and this difference could be attributed to several reasons associated with senescence, such as changed lifestyle and dietary schedule, lesser mobility, weakened immune strength, reduced intestinal and overall functionality, altered gut morphology and physiology, recurrent infections, hospitalizations, and use of medications, etc. ( Figs. 1 and 2 ). [12] It is becoming clear that an altered gut microbiota is associated with metabolic diseases in humans that range from obesity to type 2 diabetes and cardiovascular disease. [11] In mice, IL-22 has been shown to protect against metabolic disease, which further suggests a link between the altered gut microbiota, T H 17 cells and IL-22 signalling and the mediation of metabolic disease. [11] Interestingly, transplanting the gut microbiota from KD-fed mice to animals fed the control diet also raised the recipients’ seizure induction threshold levels. [15] Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice. [12] A deeper understanding of the gut microbiota, an important aspect of failing health, has the potential to contribute big gains in our understanding of metabolic health and weight loss. [11] A body of knowledge is accumulating that points to the gut microbiota as a mediator of dietary impact on the host metabolic status. [11] Mechanisms of signalling from the gut microbiota to the host The gut microbiota interacts with dietary components and metabolites to form bioactive metabolites that signal to the host through distinct mechanisms. [11] While a causal relationship has not yet been determined, the available evidences on the associations between gut microbiota, nutrition and systemic inflammation suggest that dietary interventions for positively modulating the microbiota composition and diversity could help in promoting the healthier aging and longevity. [12] The second theme is that, despite these rapid dynamics, long-term dietary habits are a dominant force in determining the composition of an individual’s gut microbiota. [11] Distinct variations in the composition of the gut microbiota in the elderly have been identified and could contribute to frailty, disease development and aging itself. [18] Trompette A, et al. Gut microbiota metabolism of dietary fiber influences allergic airway disease and hematopoiesis. [11] To move forwards, it will be essential to understand whether the gut microbiota is causally linked to host metabolism in humans. [11] Faecal microbiota transplantation, which has been shown to cure recurrent infection with Clostridium difficile 116, has also been used to directly address whether the gut microbiota can affect the metabolism of the host. [11] The gut microbiota is complex ecosystem of bacteria, fungi, and microorganisms residing in the gastrointestinal tract, which impart many health benefits onto the host. [18] Together, these observations again hint that maintaining the gut microbiota homeostasis could be beneficial for maintaining gut and overall health, whereas perturbations in gut microbiota could upset several features of host health ( Fig. 3B ). [12] Samuel BS, et al. Effects of the gut microbiota on host adiposity are modulated by the short-chain fatty-acid binding G protein-coupled receptor, Gpr41. [11] Saturated and unsaturated fats have profoundly different effects on the gut microbiota, and the altered microbiota that results from feeding unsaturated fats can offer protection from lard-induced weight gain 44. [11] In old age, the altered gut microbiota diversity and weakened gut barrier integrity may perturb the microbial and biochemical environment across the intestinal epithelial cell lining via abnormal levels of SCFAs, lipopolysaccharide (LPS), secretory Immunoglobulin A (sIgA), histamins, serotonin (5-hydroxytryptamine; 5-HT), etc. thereby instigating an abnormal (hyper) inflammatory responses eventually affecting (disturbing) the gut-brain communication. [12] Prospective studies should be performed to determine whether the gut microbiota is altered before or after the onset of disease. [11] Mechanisms that link the gut microbiota with obesity are coming to light through a powerful combination of translation-focused animal models and studies in humans. [11] It is reasonable to consider what proportion of metabolic problems in humans could be addressed by properly caring for the gut microbiota. [11] Metabolic signatures of extreme longevity in northern Italian centenarians reveal a complex remodeling of lipids, amino acids, and gut microbiota metabolism. [12] Sayin SI, et al. Gut microbiota regulates bile acid metabolism by reducing the levels of tauro-beta-muricholic acid, a naturally occurring FXR Antagonist. [11] Ridaura VK, et al. Gut microbiota from twins discordant for obesity modulate metabolism in mice. [11] The gut microbiota also interacts with the innate immune system to induce adipose inflammation, and mice that lack Toll-like receptor signalling, through loss of either of the adaptor proteins MyD88 or TRIF (also known as TICAM1), have reduced levels of inflammation in adipose tissue and are protected from insulin resistance that is induced by saturated fatty acids 44. [11] Because the gut microbiota is known to contribute to the obese phenotype, at least in mice, it might also contribute to increased adipose inflammation. [11] Studies also confirmed that the gut microbiota had to be present for the 6-Hz mice to be protected against electrically induced seizures. [15] The importance and generalizability of these initial findings are strengthened by reports of alterations in the gut microbiota of obese people 4, 13 – 15, which confer the obese or adiposity phenotypes when transferred to mice 14, 16. [11] A Specific gut microbiota dysbiosis of type 2 diabetic mice induces GLP-1 resistance through an enteric no-dependent and gut-brain axis mechanism. [12]

De Filippo C, et al. Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa. [11] From this stage onwards, diet becomes the major factor that strongly influences the subsequent maturation and maintenance of gut microbiota configuration throughout the lifespan ( Fig. 2 ). [12] Experiments that use a Western-style diet, which is devoid of fibres and rich in calories from saturated fat and sucrose, demonstrate that the gut microbiota regulates obesity through additional pathways 8. [11]

The outcomes reveal that gestational and postnatal age were associated with quantity of specific markers for gut function and maturation, as well as with composition of the gut microbiota. [16] Martínez I, et al. The gut microbiota of rural Papua New Guineans: composition, diversity patterns, and ecological processes. [11] The gut microbiota of eight hunter–gatherer or rural farming populations in various parts of the world showed increased bacterial diversity compared with those of Western populations 19, 40, 52 – 55. [11] Generally, the diversity of gut microbiota and the carriage of commensals such as bacteroides, bifidobacteria and lactobacilli are found to be reduced while the levels of opportunists such as enterobacteria, C. perfringens and C. difficile are increased in elderly. [12] Increased levels of TNF, IL-6 and IL-8 in old-age may be associated with changes in gut microbiota. [12] Gut microbes do not age per se, but the incidences of comorbidities associated with gut microbiota tend to increase as the host grows older ; even though it remains unclear whether microbiota alterations are cause or consequence of host aging ( Fig. 2 ). [12]

RANKED SELECTED SOURCES(25 source documents arranged by frequency of occurrence in the above report)

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4. (28) Antibiotic-induced changes in the microbiota disrupt redox dynamics in the gut | eLife

5. (26) Gut Microbiome: 16 Factors that can Improve or Worsen It – Selfhacked

6. (17) Food & Microbiota 2018: The first symposium will be organized in June 14 – 6th World Congress on Targeting Microbiota – October 28-30, 2018 – Porto, Portugal

7. (12) Iron supplementation has minor effects on gut microbiota composition in overweight and obese women in early pregnancy | British Journal of Nutrition | Cambridge Core

8. (11) Gastrointesinal function and microbiota development in preterm infants | Danone Nutricia Research

9. (11) Gut microbiota and cancer prevention | Healthy Living SG

10. (10) Dysbiosis and Ageing

11. (10) Microbiome | Articles

12. (10) Limitations of Feces as Proxy for Gut Microbiota | Taconic Biosciences

13. (8) Gut Bacteria and Brains: How the Microbiome Affects Alzheimer’s Disease | BrightFocus Foundation

14. (7) Gut Microbiome in Ketogenic Diet Protects against Epileptic Seizures | GEN

15. (6) Gut bacteria play key role in anti-seizure effects of ketogenic diet — ScienceDaily

16. (5) An Example of the Importance of Gut Microbiota to Aging in Flies Fight Aging!

17. (4) Changes in the Rumen Epithelial Microbiota of Cattle and Host Gene Expression in Response to Alterations in Dietary Carbohydrate Composition

18. (4) Trimethylamine N-oxide – Wikipedia

19. (3) Early Research Makes Connection Between Liver Tumor Growth Control and Gut Microbiota

20. (3) The 19th-Century Crank Who Tried to Tell Us About the Microbiome | WIRED

21. (3) Gut bacteria drive belly fat, but are genes or diet to blame?

22. (2) Triclosan, a Common Antimicrobial Ingredient in Toothpaste, Soaps, Linked to Colonic Inflammation, Altered Gut Microbiota | Office of News & Media Relations | UMass Amherst

23. (2) Demand for stool donors grows as benefits of fecal microbiota transplant are recognized

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25. (1) Research & practice – Gut Microbiota for Health