GIT

[Jo Bowyer]

http://www.californiadriedplums.org/...faq#question-1

Are dried plums the same as prunes?

Yes, they are. All prunes are plums, but not all plums are prunes. Prune plum varieties have very high sugar contents that enable them to be dried without fermenting while still containing the pits.

Why are dried plums such an effective digestive aid?

Dried plums contain both soluble and insoluble fiber as well as sorbitol, an unfermentable sugar which has been shown to produce a good medium for the production of desirable intestinal microorganisms. Insoluble fiber adds bulk and pulls water into the intestine resulting in a softer stool that is more quickly eliminated. Soluble fiber mixes with water in the stomach to become more viscous. This can result in the stomach emptying more slowly, giving a feeling of satiety, and aiding in the absorption of important nutrients.

[Jo Bowyer]

Digested wheat gluten inhibits binding between leptin and its receptor

http://www.biomedcentral.com/1471-20...ource=Teradata

Abstract

Background
Leptin resistance is considered a primary risk factor for obesity. It has been hypothesized that dietary cereal grain protein could cause leptin resistance by preventing leptin from binding to its receptor. Non-degraded dietary wheat protein has been found in human serum at a mean level of 41 ng/mL. Here, we report our findings from testing whether enzymatically digested gluten from wheat prevents leptin from binding to the leptin receptor in vitro.

Gluten from wheat was digested with pepsin and trypsin under physiological conditions. Pepsin and trypsin activity was removed from the gluten digest with a 10 kDa spin-filter or by heat treatment at 100°C for 30 min. Binding to the leptin receptor of leptin mixed with gluten digest at a series of concentrations was measured using surface plasmon resonance technology.

Results
Binding of the gluten digest to the leptin receptor was not detected. Spin-filtered gluten digest inhibited binding of leptin to the leptin receptor, with 50% inhibition at a gluten digest concentration of ~10 ng/mL. Heat-treated gluten digest did not inhibit leptin binding.

Conclusions
Digested wheat gluten inhibits binding of leptin to the leptin receptor, with half-maximal inhibition at 10 ng/mL. The inhibition is significant at clinically relevant concentrations and could therefore serve as a novel pathway to investigate to understand the molecular basis of leptin resistance, obesity and associated disorders.

Gluten intake has increased greatly over the last hundred years and has accelerated during the last few decades [14],[15]. This increase is largely due to breeding of gluten-rich cereal grain varieties and most recently by the use of extra gluten in baking and food processing to make dough easier to work and bread fluffier [15].

To assess the clinical implications of the study results, we should consider previous findings on the relationship between serum leptin and body fat mass in humans, which was found to be a strong linear or quadratic correlation (R = 0.86, P < 0.0001 for the linear correlation and R = 0.85, P < 0.001 for the quadratic correlation), as measured by underwater weighing or bioelectric impedance analysis [22],[23]. Also, another study showed that there was a linear relationship between serum leptin and cerebrospinal fluid leptin in lean individuals (R = 0.41, P < 0.05) [24]. Such correlations are of course not certain indications of a causal connection and most certainly oversimplify the mechanisms causing obesity. However, if there were a causal linear relationship between leptin level and body fat mass, a tentative 50% reduction in binding of leptin to the leptin receptor due to continual intake of cereal grain proteins would lead to a doubling of body fat mass. Furthermore, for an adult with 20% body fat mass, a doubling of body fat mass would increase body mass index (BMI) by 20%. This is the difference between current mean BMI among Swedish adults of ~25 kg/m2 and a healthier ~21 kg/m2. A corresponding BMI improvement would probably also reduce obesity-associated metabolic disorders such as dyslipidemia, cardiovascular disease, stroke, insulin resistance and type 2 diabetes in the population.

[Jo Bowyer]

Gut Microbiome of an 11th Century A.D. Pre-Columbian Andean Mummy

http://journals.plos.org/plosone/art...l.pone.0138135

Abstract

The process of natural mummification is a rare and unique process from which little is known about the resulting microbial community structure. In the present study, we characterized the microbiome of paleofeces, and ascending, transverse and descending colon of an 11th century A.D. pre-Columbian Andean mummy by 16S rRNA gene high-throughput sequencing and metagenomics. Firmicutes were the most abundant bacterial group, with Clostridium spp. comprising up to 96.2% of the mummified gut, while Turicibacter spp. represented 89.2% of the bacteria identified in the paleofeces. Microbiome profile of the paleofeces was unique when compared to previously characterized coprolites that did not undergo natural mummification. We identified DNA sequences homologous to Clostridium botulinum, Trypanosoma cruzi and human papillomaviruses (HPVs). Unexpectedly, putative antibiotic-resistance genes including beta-lactamases, penicillin-binding proteins, resistance to fosfomycin, chloramphenicol, aminoglycosides, macrolides, sulfa, quinolones, tetracycline and vancomycin, and multi-drug transporters, were also identified. The presence of putative antibiotic-resistance genes suggests that resistance may not necessarily be associated with a selective pressure of antibiotics or contact with European cultures. Identification of pathogens and antibiotic-resistance genes in ancient human specimens will aid in the understanding of the evolution of pathogens as a way to treat and prevent diseases caused by bacteria, microbial eukaryotes and viruses.

[Jo Bowyer]

N-3 Polyunsaturated Fatty Acids (PUFAs) Reverse the Impact of Early-Life Stress on the Gut Microbiota

http://journals.plos.org/plosone/art...l.pone.0139721

Abstract

Background

Early life stress is a risk factor for many psychiatric disorders ranging from depression to anxiety. Stress, especially during early life, can induce dysbiosis in the gut microbiota, the key modulators of the bidirectional signalling pathways in the gut-brain axis that underline several neurodevelopmental and psychiatric disorders. Despite their critical role in the development and function of the central nervous system, the effect of n-3 polyunsaturated fatty acids (n-3 PUFAs) on the regulation of gut-microbiota in early-life stress has not been explored.

Methods and Results

Here, we show that long-term supplementation of eicosapentaenoic acid (EPA)/docosahexaenoic acid (DHA) (80% EPA, 20% DHA) n-3 PUFAs mixture could restore the disturbed gut-microbiota composition of maternally separated (MS) female rats. Sprague-Dawley female rats were subjected to an early-life stress, maternal separation procedure from postnatal days 2 to 12. Non-separated (NS) and MS rats were administered saline, EPA/DHA 0.4 g/kg/day or EPA/DHA 1 g/kg/day, respectively. Analysis of the gut microbiota in adult rats revealed that EPA/DHA changes composition in the MS, and to a lesser extent the NS rats, and was associated with attenuation of the corticosterone response to acute stress.

Conclusions

In conclusion, EPA/DHA intervention alters the gut microbiota composition of both neurodevelopmentally normal and early-life stressed animals. This study offers insights into the interaction between n-3 PUFAs and gut microbes, which may play an important role in advancing our understanding of disorders of mood and cognitive functioning, such as anxiety and depression.

[Jo Bowyer]

Gut bacteria population, diversity linked to anorexia nervosa Studying the 'gut-brain axis,' researchers find evidence of an association

http://www.sciencedaily.com/releases...1005121310.htm

For this study, Carroll's team collected fecal samples from 16 women with anorexia nervosa after they were first admitted into the UNC Center of Excellence for Eating Disorders and then again after their weight was restored -- when they were discharged from UNC. Then Susan Kleiman, a graduate student in Carroll's lab and first author of the paper, characterized the composition and diversity of the gut microbiota in each sample.

Kleiman found significant changes in the gut bacteria populations between admission and discharge. The samples taken at clinic admission had fewer different types of bacteria, making the intestinal communities much less diverse. Microbial diversity is a sign of better overall health. Upon hospital discharge, the microbial diversity had increased, but was still significantly less diverse than that of 12 healthy individuals, whose gut microbiotas were analyzed for this study.

As the microbial communities in patients with anorexia improved during clinical care and weight gain, the moods of patients also improved. Thus, the researchers noted an association between the gut microbiota and a central symptom of people with anorexia nervosa.

The question remains whether improving microbial abundance and diversity could help relieve symptoms related to the eating disorder. To find out, Carroll formed a team of researchers including Cynthia Bulik, PhD, director of the UNC Center of Excellence for Eating Disorders; John Cryan, PhD, professor at University College Cork; Lisa Tarantino, PhD, assistant professor of psychiatry at UNC-Chapel Hill; Anthony Fodor, PhD, a bioinformatics expert at UNC-Charlotte, and Hunna Watson, PhD, a psychologist and biostatistician at UNC-Chapel Hill.

This month, they received a five-year, $2.5-million grant from the National Institutes of Mental Health to further study the relationship between the gut microbiota and anorexia nervosa.

"Over the past 10 years, prominent researchers have learned that when you take gut microbial communities of an obese person and put it in germ-free mice -- which are maintained in sterile conditions and lack intestinal microbiota -- the mice gain more weight than germ-free mice that have been colonized with a gut microbiota from a lean individual," Carroll said. "This suggests that gut microbes mediate weight gain or loss."

Other animal studies showed that adding gut bacteria to previously germ-free mice altered their behavior, especially in relation to anxiety and stress.

"We're not saying that altering gut bacteria will be the magic bullet for people with anorexia nervosa," Carroll said. "Other important factors are at play, obviously. But the gut microbiota is clearly important for a variety of health and brain-related issues in humans. And it could be important for people with anorexia nervosa."

As part of the new NIH grant, his team will characterize the microbiotas of a large number of people with anorexia nervosa as they enter UNC's clinic and when they are discharged, which typically happens when they reach about 85 percent of their ideal body weight. Then his team will put those gut bacteria in germ-free mice. This will help Carroll learn how the microbiota from anorexia nervosa patients affects the biology and behavior of the mice.

If Carroll's team learns that the bacteria has a detrimental effect on the mice, then this might suggest that cultivating a healthy microbiota could serve as a therapeutic route to help people with anorexia nervosa.

"Currently available treatments for anorexia nervosa are suboptimal," Bulik said. "In addition, the process of weight gain and renourishment can be extremely uncomfortable for patients. Often, patients are discharged from the hospital, and within months and sometimes weeks they find themselves losing weight again and facing readmission. If specific alterations in their microbiota could make renourishment less uncomfortable, help patients regulate their weight, and positively affect behavior, then we might see fewer readmissions and more cures."

[Jo Bowyer]

The pleasure of food: underlying brain mechanisms of eating and other pleasures

http://www.flavourjournal.com/content/4/1/20

Abstract

As all chefs know, great food can have a transformational impact. A great deal of recent research has gone into using the new techniques from molecular gastronomy and gastrophysics to create innovative meals with delicious original textures and flavours. These novel creations have elicited much excitement from food critiques and diners alike. Much stands to be gained if these developments were to be matched by a better understanding of how the pleasure of food comes about in the brain. This review summarises the current state-of-the-art of the science of pleasure and specifically the brain’s fundamental computational principles for eating and the pleasures evoked. It is shown how the study of food has advanced our understanding of the unitary pleasure system that is used for all pleasures. As such, these novel insights may come to serve as a guide for chefs of how to combine science and art in order to maximise pleasure—and perhaps even increase happiness.

Keywords: Dinner; Gastronomy; Brain; Pleasure cycle; Satiety; Satiation; Hedonic; Pleasure; Food; Multimodal integration; Insula; Operculum; Orbitofrontal cortex; Cingulate cortex; Wanting; Liking; Learning; Anhedonia

[Jo Bowyer]

Taste receptors in the gastrointestinal system

http://www.flavourjournal.com/content/4/1/14

Abstract

In the last 15 years, advancements in molecular biology have unraveled the proteins that function as taste receptors. There are at least five taste qualities that are consciously perceived, sweet, sour, salty, bitter, and umami. Of these five, sour and salty are mediated by ion channels, whereas the perception of sweet, umami, and bitter tastes is mediated by G protein-coupled receptors (GPCRs). These taste GPCRs belong to the TAS1R and TAS2R gene families. There are other nutrient-binding GPCRs whose taste function is still being studied such as CaSR, GPRC6A, GPR92, or GPR120. It has been suspected for more than a century that the gut can sense the chemical composition of foods. The description of multiple taste GPCRs in gastrointestinal (GI) cells suggests that there are nutrient-sensing mechanisms in the GI tract, oral, gastric, and intestinal mucosa. Oral sensing seems to mainly influence food discrimination and nutrient appetite, while post-oral chemosensors may relate to nutrient utilization and inhibition of appetite. The most common accepted view is that taste GPCRs are present in enteroendocrine cells among others also known as chemosensory cells. These cells express taste receptors and other taste-related genes. Although, functional cells of the GI mucosa that are not enteroendocrine or brush cells such as enterocytes or gastric cells may also hold receptive mechanisms that transduce the presence of certain nutrients in ingested foods and regulate gastric functions. This paper examines the importance of food chemical signals in their association with the neuroendocrine mechanisms they trigger, which are the core for metabolism and appetite regulation.

Keywords: Chemical sensing; Gut; Taste receptors; Vagus nerve; Peptide hormones; Umami; GPCRs; Cephalic phase

[Jo Bowyer]

Curcumin Mimics the Neurocognitive and Anti-Inflammatory Effects of Caloric Restriction in a Mouse Model of Midlife Obesity

http://journals.plos.org/plosone/art...l.pone.0140431

Abstract

Dietary curcumin was studied for its potential to decrease adiposity and reverse obesity- associated cognitive impairment in a mouse model of midlife sedentary obesity. We hypothesized that curcumin intake, by decreasing adiposity, would improve cognitive function in a manner comparable to caloric restriction (CR), a weight loss regimen. 15-month-old male C57BL/6 mice were assigned in groups to receive the following dietary regimens for 12 weeks: (i) a base diet (Ain93M) fed ad libitum (AL), (ii) the base diet restricted to 70% of ad libitum (CR) or (iii) the base diet containing curcumin fed AL (1000 mg/kg diet, CURAL). Blood markers of inflammation, interleukin 6 (IL-6) and C-reactive protein (CRP), as well as an indicator of redox stress (GSH: GSSG ratio), were determined at different time points during the treatments, and visceral and subcutaneous adipose tissue were measured upon completion of the experiment. After 8 weeks of dietary treatment, the mice were tested for spatial cognition (Morris water maze) and cognitive flexibility (discriminated active avoidance). The CR group showed significant weight loss and reduced adiposity, whereas CURAL mice had stable weight throughout the experiment, consumed more food than the AL group, with no reduction of adiposity. However, both CR and CURAL groups took fewer trials than AL to reach criterion during the reversal sessions of the active avoidance task, suggesting an improvement in cognitive flexibility. The AL mice had higher levels of CRP compared to CURAL and CR, and GSH as well as the GSH: GSSG ratio were increased during curcumin intake, suggesting a reducing shift in the redox state. The results suggest that, independent of their effects on adiposity; dietary curcumin and caloric restriction have positive effects on frontal cortical functions that could be linked to anti-inflammatory or antioxidant actions.

Curcumin: the Indian solid gold.
Aggarwal BB1, Sundaram C, Malani N, Ichikawa H.
Author information
Abstract

Turmeric, derived from the plant Curcuma longa, is a gold-colored spice commonly used in the Indian subcontinent, not only for health care but also for the preservation of food and as a yellow dye for textiles. Curcumin, which gives the yellow color to turmeric, was first isolated almost two centuries ago, and its structure as diferuloylmethane was determined in 1910. Since the time of Ayurveda (1900 Bc) numerous therapeutic activities have been assigned to turmeric for a wide variety of diseases and conditions, including those of the skin, pulmonary, and gastrointestinal systems, aches, pains, wounds, sprains, and liver disorders. Extensive research within the last half century has proven that most of these activities, once associated with turmeric, are due to curcumin. Curcumin has been shown to exhibit antioxidant, anti-inflammatory, antiviral, antibacterial, antifungal, and anticancer activities and thus has a potential against various malignant diseases, diabetes, allergies, arthritis, Alzheimer's disease, and other chronic illnesses. These effects are mediated through the regulation of various transcription factors, growth factors, inflammatory cytokines, protein kinases, and other enzymes. Curcumin exhibits activities similar to recently discovered tumor necrosis factor blockers (e.g., HUMIRA, REMICADE, and ENBREL), a vascular endothelial cell growth factor blocker (e.g., AVASTIN), human epidermal growth factor receptor blockers (e.g., ERBITUX, ERLOTINIB, and GEFTINIB), and a HER2 blocker (e.g., HERCEPTIN). Considering the recent scientific bandwagon that multitargeted therapy is better than monotargeted therapy for most diseases, curcumin can be considered an ideal "Spice for Life".

Available from all good supermarkets, if you can stand the taste and the off putting colour :vomit:

[Jo Bowyer]

Ecology of bacteria in the human gastrointestinal tract—identification of keystone and foundation taxa

http://microbiomejournal.biomedcentr...168-015-0107-4

Abstract

Background
Determining ecological roles of community members and the impact of specific taxa on overall biodiversity in the gastrointestinal (GI) microbiota is of fundamental importance. A step towards a systems-level understanding of the GI microbiota is characterization of biotic interactions. Community time series analysis, an approach based on statistical analysis of changing population abundances within a single system over time, is needed in order to say with confidence that one population is affecting the dynamics of another.

Results
Here, we characterize biotic interaction structures and define ecological roles of major bacterial groups in four healthy individuals by analysing high-resolution, long-term (>180 days) GI bacterial community time series. Actinobacteria fit the description of a keystone taxon since they are relatively rare, but have a high degree of ecological connectedness, and are positively correlated with diversity both within and between individuals. Bacteriodetes were found to be a foundation taxon in that they are numerically dominant and interact extensively, in particular through positive interactions, with other taxa. Although community structure, diversity and biotic interaction patterns were specific to each individual, we observed a strong tendency towards more intense competition within than between phyla. This is in agreement with Darwin’s limiting similarity hypothesis as well as a published biotic interaction model of the GI microbiota based on reverse ecology. Finally, we link temporal enterotype switching to a reciprocal positive interaction between two key genera.

Conclusions
In this study, we identified ecological roles of key taxa in the human GI microbiota and compared our time series analysis results with those obtained through a reverse ecology approach, providing further evidence in favour of the limiting similarity hypothesis first put forth by Darwin. Larger longitudinal studies are warranted in order to evaluate the generality of basic ecological concepts as applied to the GI microbiota, but our results provide a starting point for achieving a more profound understanding of the GI microbiota as an ecological system.

Keywords

Community ecology Biotic interactions Time series analysis Keystone species Foundation species Limiting similarity

[Jo Bowyer]

Disease tolerance mediated by microbiome E. coli involves inflammasome and IGF-1 signaling

http://www.sciencemag.org/content/350/6260/558

Abstract

Infections and inflammation can lead to cachexia and wasting of skeletal muscle and fat tissue by as yet poorly understood mechanisms. We observed that gut colonization of mice by a strain of Escherichia coli prevents wasting triggered by infections or physical damage to the intestine. During intestinal infection with the pathogen Salmonella Typhimurium or pneumonic infection with Burkholderia thailandensis, the presence of this E. coli did not alter changes in host metabolism, caloric uptake, or inflammation but instead sustained signaling of the insulin-like growth factor 1/phosphatidylinositol 3-kinase/AKT pathway in skeletal muscle, which is required for prevention of muscle wasting. This effect was dependent on engagement of the NLRC4 inflammasome. Therefore, this commensal promotes tolerance to diverse diseases.

http://www.sciencedaily.com/releases...1029150253.htm

In a paper published October 30, 2015 in Science, the Salk researchers reported finding a strain of micro biome Escherichia coli bacteria in mice capable of improving the animals' tolerance to infections of the lungs and intestines by preventing wasting--a common and potentially deadly loss of muscle tissue that occurs in serious infections. If a similarly protective strain is found in humans, it could offer a new avenue for countering muscle wasting, a common and deadly result of patients suffering from sepsis and hospital-acquired infections, many of which are now antibiotic resistant.

"Treatments for infection have long focused on eradicating the offending microbe, but what actually kills people aren't the bacteria themselves--it's the collateral damage it does to the body," says Janelle Ayres, a Salk assistant professor in the Nomis Foundation Laboratories for Immunobiology and Microbial Pathogenesis and senior researcher on the study.

"Our findings suggest that preventing the damage--in this case muscle wasting--can stave off the most life-threatening aspects of an infection," she adds. "And by not trying the kill the pathogen, you're not encouraging the evolution of the deadly antibiotic-resistant strains that are killing people around the world. We might be able to fight superbugs with 'superhero' bugs."

Once the most powerful and revolutionary of drugs, antibiotics appear to have reached their limits, due to the ability of bacteria to rapidly evolve resistance to the medicines. The rise of antibiotic resistance presents a grave threat to people around the world, as diseases once easily controlled repel all attempts at treatment. A recent study found that up to half of the bacteria that cause infections in US hospitals after a surgery are resistant to standard antibiotics.

In the United States alone, two million people annually become infected with bacteria that are resistant to antibiotics and at least 23,000 people die each year as a direct result of these infections, according to the U.S. Centers for Disease Control.

"Antibiotics were a huge step for medicine, but that model of killing bacteria with drugs clearly has its weaknesses," says Alexandria Palaferri Schiebe, a research associate in Ayres' lab and co-first author on the new paper. "Most researchers are looking for new antibiotics, but this fuels the arms race between doctors and bacteria. Focusing on disease tolerance--preventing harm done by the disease--instead of microbial eradication is a new paradigm of therapy for infectious diseases."

In hopes of finding new methods to counter infections, Ayres' team turned to the microbiome, the community of microbes living--typically harmoniously--within our bodies. In the human body, microbes outnumber cells by 10 to 1 and make up as much as 3 percent of body weight. Despite this, relatively little is know about how these tiny passengers interact with our development, metabolism and immune system.

Ayers began studying disease tolerance as a graduate student, hypothesizing that the gut microbiome might contain bacteria that could protect against damage caused by infections. "There is a lot of evidence to support this idea, but until now no one had identified such a strain or shown the mechanism by which a bacterium would provide disease tolerance," says Ayres.

The Salk team identified a population of laboratory mice that appeared resistant to muscle wasting. By comparing the makeup of the intestinal microbiome of these mice with mice that lacked resistance, the team identified a strain of E. coli that was present only in the wasting-resistant mice. When normal mice were given an oral treatment of this beneficial E. coli strain, they gained the ability to maintain their muscle and fat mass during intestinal infections of the bacteria Salmonella Typhimurium and pneumonia caused by the bacteria Burkholderia thailandensis.

The next step was to find out how the bacteria were conferring this tolerance to the mice. Collaborating with the laboratory of Salk Professor Ronald Evans, Ayres' team discovered that during an infection by the pathological bacteria, the E. coli left the gut and moved into the fat tissues to induce protective responses that nourish the muscles.

Normally, mice with lung and intestinal infections see a drop in a hormone known as insulin-like growth factor 1 (IGF-1), a molecule that signals the body to retain muscle mass. But the protective E. coli activated the IGF-1 pathway in the fat tissues, maintaining normal IGF-1 levels and maintaining the animal's muscle in spite of the pathogenic infections.

The Salk team further found that the E. coli strain was activating the IGF-1 muscle maintenance pathway through an intermediary, a molecular complex in cells known as the inflammasome. Part of the body's innate immune system, the inflammasome responds to an infection by triggering inflammation in the infected area to destroy the offending microbes. The E. coli used this same alarm system to tell the body to maintain IGF-1 levels and hence muscle mass.

Whether such a microbial 'superhero' could come to the rescue of humans with infections remains to be seen. Ayres' team is currently studying how long the E. coli strain can hold off the pathogens and whether the body's immune system will eventually eradicate the harmful bacteria completely. They are also beginning to examine whether such a microbe exists in humans.

"There's a lot we still need to understand, but this is a very promising sign that microbes might be used as medicine," Ayres says. "It may offer an entirely new avenue for treatment of infections, even those that are antibiotic resistant, while also preventing the rise of new resistant strains."

E. coli left the gut and moved into the fat tissues to induce protective responses that nourish the muscles.

So this begs the question as to whether a leaky gut is a protective response and how effective this attempt at protection can be. Those I have looked after for decades who have survived conditions in which they had a leaky gut have gone on to develop rheumatalogical conditions and my involvement has consisted in helping them to manage complex pain, fatigue and a compromised immune system.

[Jo Bowyer]

Comparisons of Allergenic and Metazoan Parasite Proteins: Allergy the Price of Immunity

http://journals.plos.org/ploscompbio...l.pcbi.1004546

Abstract

Allergic reactions can be considered as maladaptive IgE immune responses towards environmental antigens. Intriguingly, these mechanisms are observed to be very similar to those implicated in the acquisition of an important degree of immunity against metazoan parasites (helminths and arthropods) in mammalian hosts. Based on the hypothesis that IgE-mediated immune responses evolved in mammals to provide extra protection against metazoan parasites rather than to cause allergy, we predict that the environmental allergens will share key properties with the metazoan parasite antigens that are specifically targeted by IgE in infected human populations. We seek to test this prediction by examining if significant similarity exists between molecular features of allergens and helminth proteins that induce an IgE response in the human host. By employing various computational approaches, 2712 unique protein molecules that are known IgE antigens were searched against a dataset of proteins from helminths and parasitic arthropods, resulting in a comprehensive list of 2445 parasite proteins that show significant similarity through sequence and structure with allergenic proteins. Nearly half of these parasite proteins from 31 species fall within the 10 most abundant allergenic protein domain families (EF-hand, Tropomyosin, CAP, Profilin, Lipocalin, Trypsin-like serine protease, Cupin, BetV1, Expansin and Prolamin). We identified epitopic-like regions in 206 parasite proteins and present the first example of a plant protein (BetV1) that is the commonest allergen in pollen in a worm, and confirming it as the target of IgE in schistosomiasis infected humans. The identification of significant similarity, inclusive of the epitopic regions, between allergens and helminth proteins against which IgE is an observed marker of protective immunity explains the ‘off-target’ effects of the IgE-mediated immune system in allergy. All these findings can impact the discovery and design of molecules used in immunotherapy of allergic conditions.

[Jo Bowyer]

Gut microbiota regulates antioxidant metabolism

http://www.sciencedaily.com/releases...1106062708.htm

A recently published study shows that gut microbiota regulates the glutathione and amino acid metabolism of the host. Glutathione is a key antioxidant, found in every cell in our body. Deficiency of glutathione contributes to oxidative stress, which plays a major role in several lifestyle diseases.

The functional output and diversity of gut microbiota are important modulators for the development of various human disorders. Obesity, type 2 diabetes, atherosclerosis, non-alcoholic fatty liver disease as well as the opposite end of the spectrum, for example malnutrition, have been associated with imbalance in human gut microbiota. Hence, the interactions between the gut microbiota, host tissues of the gastrointestinal tract and other peripheral tissues as well as diet are known to be highly relevant for the health of the host.

In a recent paper published in Molecular Systems Biology, researchers at Chalmers University of Technology, the Royal Institute of Technology and the University of Gothenburg in Sweden revealed that gut microbiota regulates the glutathione and amino acid metabolism of the host. The study, highlighted on the cover of the journal, shows how a novel integrative approach can be used to reveal the metabolic differences between germ-free and conventionally raised mice through a combination of proteomics, transcriptomics and metabolomics data as well as tissue-specific metabolic modeling.

Glutathione is our body's most powerful antioxidant and the main detoxifying agent in the body. It plays a vital role in enabling the immune system, nutrient metabolism and regulation of other important cellular events. Glutathione is a very small protein, produced inside the cells from three amino acids ultimately obtained from our food or supplementation. The deficiency of glutathione contributes to oxidative stress, which plays a major role in the mechanisms of above mentioned complex disorders.

The gut microbiota modulates host amino acid and glutathione metabolism in mice
http://msb.embopress.org/content/11/10/834

[Jo Bowyer]

A distributed cell division counter reveals growth dynamics in the gut microbiota

http://www.nature.com/ncomms/2015/15...omms10039.html

Abstract

Microbial population growth is typically measured when cells can be directly observed, or when death is rare. However, neither of these conditions hold for the mammalian gut microbiota, and, therefore, standard approaches cannot accurately measure the growth dynamics of this community. Here we introduce a new method (distributed cell division counting, DCDC) that uses the accurate segregation at cell division of genetically encoded fluorescent particles to measure microbial growth rates. Using DCDC, we can measure the growth rate of Escherichia coli for >10 consecutive generations. We demonstrate experimentally and theoretically that DCDC is robust to error across a wide range of temperatures and conditions, including in the mammalian gut. Furthermore, our experimental observations inform a mathematical model of the population dynamics of the gut microbiota. DCDC can enable the study of microbial growth during infection, gut dysbiosis, antibiotic therapy or other situations relevant to human health.

[Jo Bowyer]

Immune cells make appendix 'silent hero' of digestive health

http://www.sciencedaily.com/releases...1130130021.htm

New research shows a network of immune cells helps the appendix to play a pivotal role in maintaining the health of the digestive system, supporting the theory that the appendix isn't a vestigial -- or redundant -- organ.

[Jo Bowyer]

Novel intestinal bacterium provides human gut with healthy compounds

http://www.sciencedaily.com/releases...1202084503.htm

Fibers in our food are thought to be good for health since they are converted in the intestinal tract into the favorable compound butyrate, that is crucial to maintain intestinal health. In contrast, protein is believed to be less healthy since intestinal fermentation of the building blocks of proteins, amino acids, generates undesired compounds. This latter picture is now changing since a novel intestinal bacterium has been isolated by researchers.

Production of butyrate from lysine and the Amadori product fructoselysine by a human gut commensal
http://www.nature.com/ncomms/2015/15...omms10062.html