More comprehensive human intervention studies will be essential in the future to provide insight into the potential influence of dietary polyphenols and their aromatic bacterial metabolites on intestinal microbial communities and their activities.Probiotics are defined as viable microorganisms that, when consumed in sufficient amounts, confer a health benefit on the host.To date, most of the commonly used probiotics are limited to strains of certain Lactobacillus and Bifidobacterium species . Survival during passage through the GI tract is generally considered as the essential feature for probiotics to preserve their active functions in the colon. Indeed, the probiotic strains must overcome biological barriers, including resisting gastric and bile acid secretion and tolerating intestinal lysozyme and toxic metabolites produced during digestion . Various studies found that at least a fraction of probiotic bacteria can be detected in stool for between 1 and 3 weeks after consumption . Probiotic Lactobacillus strains were also found to adapt for survival in the gut and possess gut-inducible genes that are responsive at different sites in the intestine. Interestingly, provision of the probiotic Lactobacillus plantarum to mice fed a Westernstyle diet and to humans resulted in similar gene expression profiles of this strain.As probiotics are delivered via various food vehicles, the complex food matrix should also be viewed as an important factor that may alter the probiotic activity in the gut. To date,pots with drainage holes only a few animal and clinical studies have addressed the functional roles of food on probiotic-conferred health benefits.
The mechanisms of probiotic effects on health are only partially understood but likely function either directly through interactions with host intestinal epithelial and immune cells or indirectly by modulating the indigenous intestinal microbiota. In regard to the latter, several studies have concluded that probiotic consumption does not result in global modifications of the intestinal microbiota in healthy individuals.However, probiotics might confer modest but significant changes to the functional activities of local intestinal bacterial populations. When examined at the meta-transcriptional level, intake of a probiotic fermented milk was associated with the upregulation of microbial genes corresponding to plant polysaccharide metabolism.Similarly, administration of probiotics was shown to induce crosstalk between the probiotics from the diet and the individual bacterial species in the gut and might induce competition for limited substrates that results in fluctuations tof the metabolic profile of the host.The gut microbiome of healthy adults is highly resilient , where the stable native microbiota prohibits the succession of microbes from the diet.In addition, the effect of probiotics on the gut microbiome appears to differ depending on host phenotypes such as age, health status, and chronic conditions. For example, the infant gut microbiome is highly diverse and dynamically changes during development and therefore may be easily influenced by the consumption of probiotics . In individuals with irritable bowel syndrome , probiotic consumption resulted in an increase in the numbers of Bacteroidetes in the intestine.Moreover, intake of two Lactobacillus strains by diet-induced obese mice altered microbial composition and decreased expression of inflammatory genes in the adipose tissue while increasing levels of fatty acid oxidation in the liver.Further studies are needed to investigate the effects of assorted probiotic supplements on the gut microbiome with respect to various host life stages and phenotypes.The premise behind substituting sugar with artificial sweeteners is to maintain the palatability of food at the same time as lowering energy intake.
However, a sufficiently high ingestion of non/low-digestible sugar substitutes stimulates the growth of gut microbiota and can induce transitory diarrhea in humans.In particular, the great proportion of non/low digestible sugar substitutes that reach the distal intestine are subject to fermentation by the colonic microbiota, offering approximately 2 kcal/g of energy.Although discovering and characterizing these compounds within foods is relatively new, it is of interest to note that many of these food ingredients are common in our daily diet. For example, the disaccharide alcohol maltitol is considered a common replacement for sucrose. Urinary and fecal excretions of sorbitol and maltitol after 24 h in conventional rats were shown to be minimal compared with germ-free rats.Likewise, maltitol consumption significantly increased production of SCFAs in addition to nine tested fecal microbes after a 6 week trial, including bifidobacteria, Bacteroides, Clostridium, lactobacilli, eubacteria, Atopobium, Fusobacterium prausnizii, Ruminococcus flavefaciens, and R. bromii. A 12 week administration of Splenda, composed of 1.1% of the artificial sweetener sucralose, increased fecal pH and reduced the amount of fecal bifidobacteria, lactobacilli, Bacteroides, clostridia, and total aerobic bacteria in a rat,whereas isomalt, a widely used low-energy sweetener, was considered to be bifidogenic in a human study.Overall, artificial sweetener fermentation by gut microbiota remains either unexplored or poorly documented, some of which are highlighted in a review by Payne et al.Azo compounds are widely used as coloring agents in foods, beverages, and food packaging.In addition, azo polymer coatings have been specifically designed for colon-selective drug delivery due to the presence of pH-sensitive monomers and azo cross-linking agents in the hydrogel structure. Indeed, azo dyes can be metabolized under anaerobic conditions by intestinal microbial processes and, as a result, produce the reductive cleavage products aromatic amines .
The majority of the toxic effects of azo dyes are exerted through aromatic amines produced by their colonic degradation.Raffi et al. reported that isolated intestinal bacteria in an anaerobic culture system were able to decolorize the dyes in the supernatant, suggesting that some of the azoreductase activities are extracellularly released.Xu et al. demonstrated a variable degree of efficiency in the reduction of Sudan azo dyes and Para Red by 35 prevalent human intestinal microbes in vitro.In contrast, Sudan azo dyes and their metabolites selectively inhibit the growth of some human intestinal microorganisms,which may suggest a potential impact on gut microbiome after long-term exposure. In summary, although there are tantalizing glimpses into the effect of azo dyes on microbes in vitro, more data from animal and human studies are keenly awaited.In the colon, sulfur is present in either inorganic form or organic form .The human GI tract poorly absorbs sulfate, and there is little sulfatase activity in the mucosa of the GI tract; therefore, free sulfate in the colon is likely to be of dietary origin.Dietary sulfate drives the activity of sulfate-reducing bacteria that couple oxidative phosphorylation with reduction of sulfate to produce sulfide.The total inorganic sulfur intake is much higher in the Western diet in comparison to a typical African rural diet.Highly processed foods that are high in sulfate include bread, soy flour, dried fruits, and brassicas, as well as sausage, beers, ciders, and wines.Sulfur-containing amino acids such as cysteine can be found in dietary protein and are a source of sulfur for colonic sulfate-reducing bacteria Desulfovibrio desulfuricans. Native Americans who consume a diet high in resistant starch and low in animal products harbor significantly distinct sulfate-reducing bacterial populations and more diverse and different methanogenic archaea than Americans consuming a typical Western diet.Substrate competition for hydrogen among methanogenic archaea, sulfate-reducing bacteria, acetogenic bacteria, and otherspecies likely occurs in the colon.Because hydrogen is an essential component for the survival of colonic methanogens, removal of the substrate terminates methanogenesis. Given an adequate supply of sulfate, sulfate-reducing bacteria that are more abundant in the right colon out compete methanogenic archaea for H2 due to their higher substrate affinity to produce hydrogen sulfide ,an end-product of dissimilatory sulfate reduction.As a result, the mucosal microbiome may be shaped in part through the availability of toxic sulfide compounds and the differential susceptibility of mucosalistic microbes to the toxins.Furthermore, the activity of methanogenic bacteria can also be disrupted by bile acids.In brief, methane production was thought to occur only when sulfate-reducing bacteria were not active.If sulfate is limited and hydrogen is in relative excess, methanogenic bacteria or perhaps acetogenic bacteria will become essential.Therefore, the levels of sulfate present in the colon are critical for determining which bacterial group gains a better survival advantage.Many people consume alcoholic beverages; however,drainage pot few studies exist on the effect of alcohol consumption on the gut microbiome of healthy individuals. For individuals who consume alcohol to excess, abnormal gut microbiota and bacterial overgrowth can potentially initiate or worsen alcoholinduced impaired gut barrier function and contribute to endotoxemia in patients with alcoholic fatty liver disease.
Yan et al. demonstrated a 3 week acute effect following alcohol administration in mice that resulted in bacterial overgrowth, as well as an expansion of Bacteroidetes and Verrucomicrobia bacteria while decreasing Firmicutes, with no difference observed after only 1 day or 1 weekChronic alcohol consumption induces changes in gut community profiles. For example, daily alcohol consumption for 10 weeks in a rat alters the colonic mucosa-associated bacterial microbiota fingerprint pattern.Similarly, chronic ethanol feeding for 8 weeks increased fecal pH and decreased abundance of both Bacteriodetes and Firmicutes phyla with a remarkable expansion of Proteobacteria and Actinobacteria phyla in mice.In a human trial, chronic alcohol consumption resulted in the alteration of the mucosa-associated colonic bacterial composition in a subset of alcoholics, with lower median abundances of Bacteroides and higher Proteobacteria. Furthermore, measurement of serum endotoxin suggests a change in microbial function, rather than abundance, which may lead to increased levels of gut-derived pro-inflammatory factors in chronic alcohol consumption. It is noted that the inability to detect clear differences between alcoholics with and without liver disease suggests that chronic alcohol consumption, rather than the disease physiology, is the most important event that appears to alter microbiota composition.It is now well established that host diet alters the gut microbiome. Changes in the gut microbiota composition are also considered an important factor in health and disease. Dietary assessment has provided us with a window to discover a way to reconfigure the gut microbiome. In this regard, the nutritional manipulation of the gut microbiome serves as a basis for formulating therapeutic approaches that are feasible and acceptable to the general population as a promising way to promote health in the era of personalized nutrition and medicine. Understanding the impact of foods and nutrients on host− microbe coevolution supports the essential role of a mutualistic relationship for intestinal homeostasis, but there remain challenges for nutritionists and scientific investigators alike to determine the “ideal” diet. This review collectively maintains the emerging view that diet supports a specific bacterial community structure and further suggests that a suboptimal dietary composition/quality may promote the development of diseases through introducing intestinal microbial dysbiosis. Major shifts in intestinal microbial composition are often observed when dietary differences between groups are extreme. Only a few population-wide studies are available to date, but some of them support a role of food diversity as a potential mechanism for altering gut microbial diversity. Although it is difficult to determine the causality of observed fecal microbiota shift with respect to many lifelong changes, generally, an adequate control over influential factors is important for the success of clinical studies to eliminate the drastic effects of unnecessary confounding variables. Many of the studies reviewed here rely on the assumption of equivalence between the term “fecal microbiome” and “intestinal microbiome”. Further studies are necessary to elucidate more clearly the exact impact of the selection of different diets on qualitative changes in the gut microbiota. Some nutrients that have been studied, such as dietary fiber, are a possible option for the maintenance of intestinal homeostasis and improvement of gut health, whereas others may contribute an opposite effect. Therefore, future research must be focused on looking to improve the effectiveness of diets with an underlying long-term “targeted approach” that allows improvement of intestinal microbial composition and functional activities. In other instances, when dietary differences are small and on a short time scale, gut microbiota changes are not as obvious, but that is not to say that changes do not occur. An alteration of the gut microbiota at lower taxonomic levels is still likely to have important functional consequences for the host. Notably, gut microbiota varies dramatically from individual to individual in lower taxonomic levels. Even small dietary changes may have impacts on the gut microbiota and altered metabolic activities in the microbial profile that are not easily detected by the phylogenetic/taxonomic methods. Metabolic alterations induced by diet may result in varying the microbial capability of synthesizing substances in the intestinal tract. It appears that measurement of bacterial enzyme activities may be a more sensitive indicator of diet induced changes in the gut microbiota than taxonomic-based methods.