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So, I recently came up with this question. I googled it, but couldn't understand the proper functions of E-coli bacteria. A little definition would be wonderful.
Nonpathogenic E.coli are a component of the gut microbiome of humans and many other organisms.
They are commensals, meaning that when they remain in the areas they have evolved to live in, and when they do not acquire virulence factors, they are benign. They live in our digestive tract and basically do nothing to harm us.
In fact, commensal microorganisms like E.coli can be considered part of the multicellular organisms innate immune system. They take up space on the exposed surfaces of internal organs such as the intestines and prevent the colonization of pathogenic strains of microorganisms.
Along with the endothelial cells and mucous, commensals form the barrier defenses that are the first line of protection against pathogenic organisms. Basically they are the good neighbors that don't cause problems and they don't leave space for bad neighbors to move in.
Problems can occur if they gain access to areas that are normally sterile. If the intestine is perforated and E.coli gain access to the thoracic cavity, they can become an opportunistic pathogen, as they will not be interacting with the host in a way that can control their proliferation. They can also come in contact with cells that are not expressing the necessary proteins to protect them from the E.coli.
You can also end up with the situation where a pathogenic bacteria or a bacteriophage carrying a virulence factor can transfer that virulence factor to the commensal E.Coli, turning them pathogenic.
But for the most part E.coli are there to take up space that could otherwise be colonized by harmful bacteria.
E. coli do not serve a human function but live inside our digestive system because our bodies can't prevent bacteria like them from living there. They live there because they can prosper and reproduce there. Most strains of E. coli do not cause problems for us, and by being part of the normal bacterial population in our gut they out-compete other, potentially more harmful bacteria and keep them suppressed. E. coli mainly live in the large intestine, not the stomach.
E. Coli bacteria are present in the caecum region of large intestine and plays a major role in erythropoeisis i. e. Formation of RBCs.
How E. coli passes safely through stomach acid
In some parts of the world, many small children become infected with severe diarrhea which often proves fatal. The condition is usually caused by strains of Escherichia coli (commonly known as E. coli) bacteria, and bacteria of the genus Yersinia. These bacteria attach themselves to the wall of the small intestine and use a needle-like apparatus to inject toxins into the tissue. Yet these bacteria usually enter the human body via the mouth – and you would expect them to be killed off by the strong acid in the stomach, which provides a barrier against infection.
Members of the collaborative research center "The Bacterial Cell Envelope" at the University of Tübingen including researchers from the Tübingen University Hospitals as well as Jack C. Leo and Professor Dirk Linke of the Max Planck Institute for Developmental Biology investigated this phenomenon and discovered how these bacteria can protect themselves from acid and mechanical stress as they pass through the stomach. The results were published in the latest issue of Molecular Microbiology.
E. coli and Yersinia bacteria attack cells in the small intestine which absorb nutrients. They use adhesins such as intimin (a protein the name comes from "intimate adherence") to stick to intestinal epithelial cells and to subsequently form tiny channels between the bacteria and the intestinal cells. In this way they are able to introduce diarrhea-causing toxins into the intestine.
The intimin is inserted into the bacterial cell envelope, where it binds with the bacteria´s stabilizing structure, peptidoglycan, a mesh-like molecule consisting of sugars and amino acids. "But the binding of intimin with peptidoglycan only works under acid conditions," says Dirk Linke. "We assume that this mechanism protects against acidic and mechanical stress and that E. coli bacteria can pass through the stomach unharmed." Intimin therefore supports the infection process by bacteria which would otherwise have difficulty reaching the small intestine. The researchers suspect that intimin boosts the bacteria's virulence.
How many bacteria in gut?
Scientists reveal the human gut turns out to store a lot of bacteria. Unmitigated, there are about 2,000 bacteria living in the gut.
Scientists from the Wellcome Sanger Institute and the European Molecular Biology Laboratory – European Bioinformatics Institute (EMBL-EBI), identified thousands of unknown microbes in the intestine.
Scientists used a method of studying genetic material from human gut samples, known as metagenomics.
The method of reconstructing the collection of bacteria and putting it together in the form of an image to be identified.
For further processing, scientists are also utilizing a special tool detecting the composition of gut bacteria from around the world.
However, scientists need to take longer to be able to identify the type of bacteria that is in the human intestine.
Development of the human GI microbiota
The development of the microbiota is generally believed to begin from birth, although this dogma is challenged by a limited number of studies in which microbes were detected in womb tissues, such as the placenta [23,24]. After birth, the GI tract is rapidly colonised, with life events such as illness, antibiotic treatment and changes in diet causing chaotic shifts in the microbiota [24,25]. The mode of delivery also appears to affect the microbiota composition, with vaginally delivered infants' microbiota containing a high abundance of lactobacilli during the first few days, a reflection of the high load of lactobacilli in the vaginal flora [26,27]. In contrast, the microbiota of infants delivered by C-section is depleted and delayed in the colonisation of the Bacteroides genus, but colonised by facultative anaerobes such as Clostridium species [28,29]. Whilst the faecal microbiota of 72% of vaginally delivered infants resembles that of their mothers' faecal microbiota, in babies delivered by C-section, this percentage is reduced to only 41% . In early stages of development, the microbiota is generally low in diversity and is dominated by two main phyla, Actinobacteria and Proteobacteria [24,31]. During the first year of life, the microbial diversity increases and the microbiota composition converges towards a distinct adult-like microbial profile with temporal patterns that are unique to each infant . By around 2.5 years of age, the composition, diversity and functional capabilities of the infant microbiota resemble those of adult microbiota [24,25]. Although, in adulthood, the composition of the gut microbiota is relatively stable, it is still subject to perturbation by life events . In individuals over the age of 65, the microbial community shifts, with an increased abundance of Bacteroidetes phyla and Clostridium cluster IV, in contrast with younger subjects where cluster XIVa is more prevalent . In contrast, a separate study observed that the microbiota of a young cohort and an elderly population (70 years) were relatively comparable, whilst the diversity of the microbiota from a cohort of centenarians was significantly reduced . The centenarian microbiota also exhibited group-specific differences such as an increase in the abundance of facultative anaerobes (e.g. Escherichia coli) and rearrangement of the profile of butyrate producers (e.g. decrease in Faecalibacterium prausnitzii) . In the elderly population, a significant relationship has been identified between diversity and living arrangements, such as community dwelling or long-term residential care . Overall, the capacity of the microbiota to carry out metabolic processes such as short-chain fatty acid (SCFA) production and amylolysis is reduced in the elderly, whilst proteolytic activity is increased . Given the increasing evidence for the role of SCFAs as key metabolic and immune mediators (as reviewed below), it was postulated that the decrease in SCFAs may nurture the inflamm-ageing process in the intestine of aged people .
Could gut bacteria neutralize our American diets?
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A specific strain of human gut bacteria breaks down the chemical fructoselysine and turns it into harmless byproducts, according to new research in mice.
The study sheds light on how human gut microbes break down processed foods—especially potentially harmful chemical changes that modern food manufacturing processes often produce.
Eating processed foods such as breads, cereals, and sodas is associated with negative health effects, including insulin resistance and obesity.
Fructoselysine is in a class of chemicals called Maillard Reaction Products, which form during food processing. Some of these chemicals have been linked to harmful health effects. These findings raise the prospect that it may be possible to use knowledge of the gut microbiome to help develop healthier, more nutritious processed foods.
Gut bacteria and our modern diets
Researchers conducted the study in mice that they raised under sterile conditions, gave known collections of human gut microbes, and fed diets containing processed food ingredients.
“This study gives us a deeper view of how components of our modern diets are metabolized by gut microbes, including the breakdown of components that may be unhealthy for us,” says Jeffrey I. Gordon, professor and director of the Edison Family Center for Genome Sciences & Systems Biology at Washington University School of Medicine in St. Louis.
“We now have a way to identify these human gut microbes and how they metabolize harmful food chemicals into innocuous byproducts.”
Human gut microbial communities see foods as collections of chemicals. Some of these chemical compounds have beneficial effects on the communities of microbes living in the gut as well as on human health. For example, Gordon’s past work has shown that the gut microbiome plays a vital role in a baby’s early development, with healthy gut microbes contributing to healthy growth, immune function, and bone and brain development.
Modern food processing can generate chemicals that may be detrimental to health. Such chemicals have been associated with inflammation linked to diabetes and heart disease. The researchers are interested in understanding the complex interactions between human gut microbes and the chemicals that people commonly consume as part of a typical American diet.
In the study, the researchers showed that a specific bacterium called Collinsella intestinalis breaks down the chemical fructoselysine into components that are harmless.
“Fructoselysine is common in processed food, including ultra-pasteurized milk, pasta, chocolate, and cereals,” says first author Ashley R. Wolf, a postdoctoral researcher in Gordon’s lab. “High amounts of fructoselysine and similar chemicals in the blood have been linked to diseases of aging, such as diabetes and atherosclerosis.”
A unique strain
When researchers fed them a diet containing high amounts of fructoselysine, mice harboring Collinsella intestinalis in their gut microbial communities showed an increase in the abundance of this bacteria as well as an increase in the gut microbial communities’ ability to break down fructoselysine into harmless byproducts.
“This specific bacterial strain thrives in these circumstances,” Gordon says. “And as it increases in abundance, fructoselysine is metabolized more efficiently.”
He adds, “The new tools and knowledge gained from this initial study could be used to develop healthier, more nutritious foods as well as design potential strategies to identify and harness certain types of gut bacteria shown to process potentially harmful chemicals into innocuous ones. A corollary is that they may help us distinguish between consumers whose gut microbial communities are either vulnerable or resistant to the effects of certain products introduced during food processing.”
Emphasizing the complexity of this task, Gordon, Wolf, and their colleagues also showed that close cousins of Collinsella intestinalis did not respond to fructoselysine in the same way. These bacterial cousins, whose genomes vary somewhat, do not thrive in a fructoselysine-rich environment.
The researchers say future studies are necessary before scientists will be able to identify and harness the specific capacities of individual microbes to clean up the array of potentially deleterious chemicals produced during some types of modern food manufacturing.
The study appears in the journal Cell Host & Microbe. Support for the work came from the National Institutes of Health, the American Diabetes Association, the Damon Runyon Cancer Research Foundation, and the Russian Science Foundation.
Gordon is a cofounder of Matatu Inc., a company characterizing the role of diet-by-microbiota interactions in animal health.
COMPOSITION OF THE NORMAL GUT MICROBIOTA
Even though it was earlier thought that the gut microbiota comprised of 500-1000 species of microbes a recent large scale study has estimated that the collective human gut microflora is composed of over 35000 bacterial species. Furthermore, if defined from a perspective of total bacterial genes, the Human Microbiome Project and the Metagenome of the Human Intestinal tract (MetaHIT) studies suggest that there could be over 10 million non-redundant genes in the human microbiome. A Danish study of the gut microbiome and their function involving 123 non-obese and 169 obese individuals resulted in the concept of high gene count (HGC) and low gene count (LGC), both of which have implications in health and disease. The HGC microbiome includes Anaerotruncus colihominis, Butyrivibrio crossotus, Akkermansia sp., and Fecalibacterium sp. with a high Akkermansia (Verrucomicrobia): Ruminococcus torque/gnavus ratio. The defining features of HGC microbiome in favour of a digestive health includes increased proportion of butyrate producing organisms, increased propensity for hydrogen production, development of a methanogenic/acetogenic ecosystem and reduced production of hydrogen sulfide. The HGC individuals have a functionally much robust gut microbiome and lower prevalence of metabolic disorders and obesity. On the other hand, LGC individuals harbor a higher proportion of pro-inflammatory bacteria such as Bacteroides and Ruminococcus gnavus, both of which are known to be associated inflammatory bowel disease[20,21]. Other members of LGC bacteria include Parabacteroides, Campylobacter, Dialister, Porphyromonas, Staphylococcus and Anaerostipes. In addition, few of the key bacterial metabolites in LGC individuals include modules for β-glucuronide degradation, degradation of aromatic amino acids, and dissimilatory nitrite reduction, all of which are known to have deleterious effects.
Overall, the healthy gut microbiota is predominantly constituted by the phyla Firmicutes and Bacteroidetes. This is followed by the phyla Actinobacteria and Verrucomicrobia. Even though this general profile remains constant, gut microbiota exhibits both temporal and spatial differences in distribution at the genus level and beyond. As one travels from the esophagus distally to the rectum, there will be a marked difference in diversity and number of bacteria ranging from 10 1 per gram of contents in the esophagus and stomach to 10 12 per gram of contents in the colon and distal gut. Figure Figure2 2 depicts the temporal diversity of the gut microbiota as one travels from the esophagus distally to the colon. Streptococcus appears to be the dominant genus in the distal esophagus, duodenum and jejunum[23,24]. Helicobacter is the dominant genera present in the stomach and determines the entire microbial landscape of the gastric flora, i.e., when Helicobacter pylori (H. pylori) inhabits the stomach as a commensal, there is a rich diversity constituted by other dominant genus such as Streptococcus (most dominant), Prevotella, Veillonella and Rothia[25,26]. This diversity shrinks once H. pylori acquire a pathogenic phenotype. The large intestine constitutes of over 70% of the all microbes found in the body, and gut flora that is generally discussed in the context of disease state by and large implies the colonic flora (especially those derived from stool metagenomic data). The predominant phyla that inhabit the large intestine include Firmicutes and Bacteroidetes. Traditionally, the Firmicutes: Bacteroidetes ratio has been implicated in predisposition to disease states. However, the significant variability even in healthy individuals that has been observed across recent studies makes the relevance of this ratio debatable. Besides genera from phyla Firmicutes and Bacteroidetes, human colon also harbors primary pathogens, e.g., species such as Campylobacter jejuni, Salmonella enterica, Vibrio cholera and Escherichia coli (E. coli), and Bacteroides fragilis, but with a low abundance (0.1% or less of entire gut microbiome)[6,28]. The abundance of the phylum Proteobacteria is markedly low and its absence along with high abundance of signature genera such as Bacteroides, Prevotella and Ruminococcus suggests a healthy gut microbiota. Besides this longitudinal difference, there also exists an axial difference from the lumen to the mucosal surface of the intestine. While Bacteroides, Bifidobacterium, Streptococcus, Enterobacteriacae, Enterococcus, Clostridium, Lactobacillus and Ruminococcus are the predominant luminal microbial genera (can be identified in stool), only Clostridium, Lactobacillus, Enterococcus and Akkermansia are the predominant mucosa and mucus associated genera (detected in the mucus layer and epithelial crypts of the small intestine).
Distribution of the normal human gut flora.
The other way of classifying the gut flora, as proposed by the MetaHIT Consortium, is based on species composition which cluster into well-balanced host-microbial symbiotic states that is stable over geography and gender, but can respond differently to diet and drugs. These clusters have been named enterotypes. Interestingly, the abundance of molecular functions however may not correlate with abundance of species within the enterotypes. Furthermore, as shown in a recent study on the association of gut microbiome with atherosclerosis, there may not be significant changes in the enterotype observed in disease conditions. There are broadly three enterotypes, namely: Enterotype 1, which has a high abundance of Bacteroides Enterotype 2, which has high abundance of Prevotella and Enterotype 3 which has high abundance of Ruminococcus. The bacteria belonging to Enterotype 1 have a wide saccharolytic potential, as evidenced by the presence of genes that code for enzymes such as proteases, hexoaminidases and galactosidases. In view of these set of enzymatic potential, it appears likely that these organisms derive energy from dietary carbohydrates and proteins. Enterotype 2 behave predominantly as a degrader of the mucin glycoproteins that line the gut mucosal layer. Enterotype 3 also is associated with mucin degradation, in addition to membrane transport of sugars. The enterotypes also possess other specific metabolic functions. For instance, biotin, riboflavin, pantothenate and ascorbate synthesis are more abundantly seen in enterotype 1 while thiamine and folate synthesis are more predominant in enterotype 2. However, the concept of enterotyping does not explain the relative distribution of different classes of organisms in different individuals. Since Bacteroides and Prevotella do not exist in equal proportion in the gut, the concept of enterogradient based upon the dominance of either of these two organisms could be another defining concept. This could explain the inter-individual distribution at the class level in a better way.
Diagnosis and treatment
Doctors diagnose E. coli infections by testing stool samples for the bacteria and specific toxins, according to the Mayo Clinic.
E. coli infections aren't typically treated with antibiotics unless the infection is outside the intestinal tract, such as with a UTI. Within the intestinal tract, though, "antibiotics may kill other beneficial bacteria in the gut, allowing more space and nutrients for the E. coli to grow," said Sarah Fankhauser, a microbiologist at Oxford College of Emory University in Georgia.
Doctors also recommended against taking anti-diarrheal medication to treat the symptoms of the infection, as the medication can slow down the digestive system and prevent the body from removing the toxins produced by the E. coli. Instead, most adults who are otherwise healthy typically recover from the infection in about a week with rest and proper hydration.
Functions of Alimentary Tract (With Diagram)
In most of the cases of foodborne illness we consider, the pathogenic (disease producing) effect occurs in the alimentary tract giving rise to symptoms such as diarrhoea and vomiting. Since these are essentially a dysfunction of the gut, a useful starting point would be to outline its normal operation and the role micro organisms play in this process.
The alimentary or gastrointestinal tract is not an internal organ of the body but a tube passing through it from the mouth to the anus (Figure 6.6). Its principal functions are the digestion and absorption of food and the excretion of waste.
Unlike most of the body’s other external surfaces, it is not lined with a dry protective skin and so, although it possesses some protective features, it offers a more congenial environment for micro-organisms and an easier route by which they can penetrate the body.
In the mouth, food is mixed with saliva and broken down mechanically to increase the surface area available for attack by digestive enzymes. Saliva is an alkaline fluid containing starch-degrading (amylase) enzyme and the antimicrobial factors immunoglobulin (IgA), lysozyme, lactoferrin and lacto peroxidase.
It provides lubrication to assist chewing and swallowing and performs a cleansing function, rinsing the teeth and mouth to remove debris. On average, an adult secretes and swallows about 1.5 1 of saliva each day.
The variety of foods consumed and the range of micro-environments in the mouth result in a diverse and continually changing microflora. On the teeth, bacteria are associated with the formation of dental plaque – an organic film in which bacteria are embedded in a matrix derived from salivary glycoproteins and microbial polysaccharides.
The microbial composition of plaque varies with its age but filamentous Fusobacterium species and streptococci are common components. Plaque offers a protective environment for bacteria and its development is often a prelude to conditions such as dental caries and periodontal disease.
Swallowed food descends via the oesophagus into the stomach a bulge in the alimentary tract which serves as a balance tank from which food is gradually released into the small intestine for further digestion.
In the stomach, food is blended with gastric juice, an acidic fluid containing hydrochloric acid. This has a marked effect on ingested micro-organisms, killing most. Normally only acid-tolerant vegetative cells and spores survive and the microbial count in the stomach is low, although lactobacilli are frequently found in association with the stomach wall.
Gastric acidity generally provides very effective protection for subsequent sections of the intestine but is not, as we shall see, an invulnerable defence.
Bacteria can evade prolonged exposure to the acid by being sheltered in food particles or as a result of accelerated passage through the stomach as occurs, for instance, when the stomach is full. Alternatively, acidity may be neutralized by the food or absent as a result of illness.
The digestive functions of the stomach are not confined to those of a mechanical churn with antimicrobial features. Proteases, such as pepsin, and lipase which can operate at low pH partially digest the stomach contents. The gastric mucosa also secretes a protein responsible for efficient absorption of vitamin B12.
Little absorption of nutrients occurs in the stomach, with the notable exception of ethanol, but some material transfer is often necessary to adjust the osmotic pressure of the stomach contents to ensure they are isotonic with body fluids.
From the stomach, small quantities of the partially digested mixture of food and gastric juice, known as chyme, are released periodically into the small intestine. In this muscular tube over 6 metres long most of the digestion and absorption of food occur.
Its internal lining is extensively folded and the folds covered with finger-like projections or villi which are themselves covered in microvilli. This gives the inner surface the appearance and texture of velvet and maximizes the area available for absorption (Figure 6.6).
In the first section of the small intestine, the duodenum, large-scale digestion is initiated by mixing the chyme with digestive juice from the pancreas and bile from the gallbladder which neutralize the chyme’s acidity. The pancreatic juice also supplies a battery of digestive enzymes, and surfactant bile salts emulsify fats to facilitate their degradation and the absorption of fat soluble vitamins.
Further digestive enzymes that break down disaccharides and peptides are secreted by glands in the mucous lining of the duodenum called, with evocations of a Gothic horror, the crypts of Lieberkuhn.
The duodenum is a relatively short section of the small intestine, accounting for only about 2% of its overall length. Food is swept along by waves of muscle contraction, known as peristalsis, from the duodenum into the jejunum and thence into the ileum.
During this passage, nutrients such as amino acids, sugars, fats, vitamins, minerals and water are absorbed into capillaries in the villi from where they are transported around the body. Absorption is sometimes a result of passive diffusion, but more often involves the movement of nutrients against a concentra­tion gradient an active process entailing the expenditure of energy.
The microbial population increases down the length of the small intestine: counts of 10 2 -10 3 ml -1 in the duodenum increase to around 10 3 -10 4 in the jejunum, 10 5 in the upper ileum and 10 6 in the lower ileum. This corresponds with a decreasing flux of material through the small intestine as water is absorbed along its length.
In the higher reaches of the duodenum, the flow rate is such that its flushing effect frequently exceeds the rate at which micro-organisms can multiply so that only those with the ability to adhere to the intestinal epithelium can persist for any length of time.
As the flow rate decreases further along the small intestine, so the microbial population increases, despite the presence of antimicrobial factors such as lysozyme, secretory immunoglobulin, IgA, and bile.
In the healthy individual, the microflora of the small intestine is mainly comprised of lactobacilli and streptococci, although, as we shall see, other bacteria have the ability to colonize the epithelium and cause illness as a consequence.
Extensive microbial growth takes place in the colon or large intestine where material can remain for long periods before expulsion as faeces.
During this time active absorption of water and salts helps to maintain the body’s fluid balance and to dry faecal matter. Bacterial cells account for 25-30% of faeces, amounting to 10 10 -10 11 cfu g -1 the remainder is composed of indigestible components of food, epithelial cells shed from the gut, minerals, and bile.
Obligate anaerobes such as Bacteroides and Bifidobacterium make up 99% of the flora of the large intestine and faeces. Members of the Enterobacteriaceae, most commonly Escherichia coli, are normally present at around 10 6 g -1 , enterococci around 10 5 g -1 , Lactobacillus, Clostridium and Fusobacterium, 10 3 -10 5 g -1 , plus numerous other organisms, such as yeasts, staphylococci and pseudomonads, at lower levels.
The interaction between the gut microflora and its host appears to have both positive and negative aspects and is the subject of much current research and conjecture. Addition of antibiotics to feed has been shown to stimulate the growth of certain animals, suggesting that some gut organisms have a deleterious effect on growth.
A normal gut microflora confers some protection against infection. One example of this effect is the inflammatory disease pseudomembranous colitis caused by Clostridium difficile.
Normally the organism is present in the gut in very low numbers, but if the balance of the flora is altered by antibiotic therapy, it can colonize the colon releasing toxins. Similarly, the infective doses of some other enteric pathogens have been shown to be lower in the absence of the normal gut flora.
It appears that protection is not simply a result of the normal flora occupying all available niches, since entero-toxigenic E. coli adheres to sites that are normally vacant. Some direct antagonism through the production of organic acids and bacteriocins probably plays a part, but stimulation of the host immune system and its capacity to resist infection also appear to be factors.
In monogastric animals such as humans, gut micro-organisms do not play the same central role in host nutrition as they do in ruminants.
Some facultative anaerobes found in the gut, such as E. coli and Klebsiella aero-genes are known to produce a variety of vitamins in vitro and studies using animals reared in a germ-free environment and lacking any indigenous microflora have shown that in vivo vitamin production by micro-organisms can be important on certain diets.
In humans, however, the evidence is less convincing. Some have questioned the efficiency of absorption of vitamins produced in the large intestine pointing to the fact that vegans have developed vitamin B12 deficiency despite its production in the gut and excretion in the faeces.
It appears that an adequate balanced diet will probably meet all the body’s requirements in this respect and that, short of coprophagy, access to vitamins produced in situ is limited.
What Is the Symbiotic Relationship Between E. Coli and Humans?
Symbiosis is defined as a long-term or close relationship between two or more organisms of different species. Therefore, the relationship between E. coli (Escherichia coli) and humans can be described as mutualistic. This means that both the E. coli and its human host benefit from the bacteria residing in the intestinal tract.
The human body provides E. coli with a safe, enclosed, and comfortable living environment in which the bacteria receive the required nutrients for reproduction and growth, and carry out several necessary functions. E. coli, in turn, makes it possible for humans to absorb vital nutrients, including Vitamin K, through the colon. For this reason, it is considered an essential organism in the human body.
While humans and E. coli maintain a symbiotic relationship in which E. coli inhabits the gut, some strains of the bacteria, specifically E. coli O157:H7, can cause serious illness and even death when ingested. E. coli can live independently outside a host if the conditions are right, lurking in fecal matter, in warm environments or on poorly washed produce. E. coli's negative effects on humans have three main manifestations: urinary tract infections, neonatal meningitis and gastroenteritis, none of which are pleasant, and some of which can become deadly.
Engineered bacteria to report gut function: technologies and implementation
The human gut microbiota interacts extensively with the host and is intricately linked to health and disease.
Non-invasive tools to monitor microbial states and disease biomarkers in the gut are lacking.
Engineered bacteria sense and respond to external signals and can function as reporters of the gut environment.
Emerging technologies will help create diagnostic bacteria that can monitor and respond to multiple signals in vivo.
Advances in synthetic biology and microbiology have enabled the creation of engineered bacteria which can sense and report on intracellular and extracellular signals. When deployed in vivo these whole-cell bacterial biosensors can act as sentinels to monitor biomolecules of interest in human health and disease settings. This is particularly interesting in the context of the gut microbiota, which interacts extensively with the human host throughout time and transit of the gut and can be accessed from feces without requiring invasive collection. Leveraging rational engineering approaches for genetic circuits as well as an expanding catalog of disease-associated biomarkers, bacterial biosensors can act as non-invasive and easy-to-monitor reporters of the gut. Here, we summarize recent engineering approaches applied in vivo in animal models and then highlight promising technologies for designing the next generation of bacterial biosensors.