Posts Tagged ‘microbiome’


The research has presented strong evidence that Parkinson’s disease begins in the gastrointestinal tract and spreads via the vagus nerve to the brain. Many patients have also suffered from gastrointestinal symptoms before the Parkinson’s diagnosis is made. The image is for illustrative purposes only.

A major epidemiological registry-based study from Aarhus University and Aarhus University Hospital indicates that Parkinson’s disease begins in the gastrointestinal tract; the study is the largest in the field so far.

The chronic neurodegenerative Parkinson’s disease affects an increasing number of people. However, scientists still do not know why some people develop Parkinson’s disease. Now researchers from Aarhus University and Aarhus University Hospital have taken an important step towards a better understanding of the disease.

New research indicates that Parkinson’s disease may begin in the gastrointestinal tract and spread through the vagus nerve to the brain.

“We have conducted a registry study of almost 15,000 patients who have had the vagus nerve in their stomach severed. Between approximately 1970-1995 this procedure was a very common method of ulcer treatment. If it really is correct that Parkinson’s starts in the gut and spreads through the vagus nerve, then these vagotomy patients should naturally be protected against developing Parkinson’s disease,” explains postdoc at Aarhus University Elisabeth Svensson on the hypothesis behind the study.

A hypothesis that turned out to be correct:

“Our study shows that patients who have had the the entire vagus nerve severed were protected against Parkinson’s disease. Their risk was halved after 20 years. However, patients who had only had a small part of the vagus nerve severed were not protected. This also fits the hypothesis that the disease process is strongly dependent on a fully or partially intact vagus nerve to be able to reach and affect the brain,” she says.

The research project has just been published in the internationally recognised journal Annals of Neurology.

The first clinical examination

The research has presented strong evidence that Parkinson’s disease begins in the gastrointestinal tract and spreads via the vagus nerve to the brain. Many patients have also suffered from gastrointestinal symptoms before the Parkinson’s diagnosis is made.

“Patients with Parkinson’s disease are often constipated many years before they receive the diagnosis, which may be an early marker of the link between neurologic and gastroenterologic pathology related to the vagus nerve ,” says Elisabeth Svensson.

Previous hypotheses about the relationship between Parkinson’s and the vagus nerve have led to animal studies and cell studies in the field. However, the current study is the first and largest epidemiological study in humans.

The research project is an important piece of the puzzle in terms of the causes of the disease. In the future the researchers expect to be able to use the new knowledge to identify risk factors for Parkinson’s disease and thus prevent the disease.

“Now that we have found an association between the vagus nerve and the development of Parkinson’s disease, it is important to carry out research into the factors that may trigger this neurological degeneration, so that we can prevent the development of the disease. To be able to do this will naturally be a major breakthrough,” says Elisabeth Svensson.

https://neurosciencenews.com/parkinsons-gastrointestinal-tract-neurology-2150/

Advertisements

by MIKE MCRAE

Transforming the microbial environment in the guts of children diagnosed with autism could significantly ease the severity of their condition’s signature traits, according to newly published research.

A study on the effects of a form of faecal transplant therapy in children on the autism spectrum found participants not only experienced fewer gut problems, but continued to show ongoing improvements in autism symptoms two years after the procedure.

Arizona State University researchers had already discovered a dose of healthy gut microflora caused characteristics associated with autism spectrum disorder (ASD) to ease or vanish for at least a couple of months after treatment ended.

But to be taken seriously as a potential therapy, there needed to be long term improvements. So a return to the original group of volunteers for another check-up was in order.

It turned out those new microbes were settling in nicely.

“In our original paper in 2017, we reported an increase in gut diversity together with beneficial bacteria after microbiota transfer therapy (MTT), and after two years, we observed diversity was even higher and the presence of beneficial microbes remained,” says biotechnologist Dae-Wook Kang.

The gut might seem like an odd place to start in developing therapies that assist individuals with a neurological condition such as autism.

But in addition to its defining characteristics of impaired social and communication skills, sensory challenges, and reduced core strength and motor control, for up to half of those with ASD the condition can come with a bunch of gut problems.

“Many kids with autism have gastrointestinal problems, and some studies, including ours, have found that those children also have worse autism-related symptoms,” says environmental engineer Rosa Krajmalnik-Brown.

Previous studies have repeatedly pointed to the potential benefits of swapping out a ‘bad’ microbial communities for a better one, either through using probiotics or courses of antibiotics.

Most showed promising short-term effects, suggesting there was more to be explored when it comes to gut-based therapies.

“In many cases, when you are able to treat those gastrointestinal problems, their behaviour improves,” says Krajmalnik-Brown.

In an attempt to elicit a more long-term result, the researchers pulled out the big guns. Forget dropping in a few microbial tourists or killing off a handful of trouble-makers – they went for a whole mass migration.

Using a customised process of gut microflora transplantation called microbiota transfer therapy, the researchers gave 18 kids aged between 7 and 16 a belly full of new microorganisms.

All of the volunteers had both an autism diagnosis and moderate to severe gastrointestinal problems. This group was compared with 20 equivalent control subjects who had neither gut problems nor an ASD diagnosis.

Both were treated for 10 weeks and then had follow-up test sessions for a further 8 weeks.

Admittedly, the experiment wasn’t blinded, so we do need to be cautious in how we read into the results. Placebo effects can’t be ruled out in cases like this.

But saying they were ‘promising’ isn’t too strong a claim to make. The children not only experienced an 80 percent reduction in gastrointestinal symptoms, they showed significant improvements when tested with common ASD diagnostic tools.

Two years later, those same tests indicate the conditions have only improved.

“The team’s new publication reports that the study demonstrated that two years after treatment stopped the participants still had an average of a 58 percent reduction in GI symptoms compared to baseline,” says Krajmalnik-Brown.

“In addition, the parents of most participants reported a slow but steady improvement in core ASD symptoms.”

An external evaluation using a standard ASD diagnostic tool concluded 83 percent of the initial test group could be considered as severe on the autistic spectrum. Two years later, this dropped to just 17 percent.

Amazingly, 44 percent no longer made the cut-off for being on the mild end of the spectrum at all.

Overall, the evaluator determined the severity of ASD traits was reduced by 47 percent compared with their baseline.

For a therapy that has barely any side-effects, and such remarkable improvements in challenges many with ASD struggle with, it’s surely a treatment that will continue to attract attention for further research.

Faecal transplants might sound a little gross, but you might as well get used to them. We’re bound to be seeing them used for a variety of things in the future, from treating superbugs to winning sports.

Now that we’re learning our neurological health is intimately connected with our digestive system, transplanting microbial communities from a healthy gut is seen as the next big thing in treating brain disorders.

This isn’t to say microflora cause autism. It’s a complex condition that has its roots in a diverse range of genes and environmental influences that nudge the brain’s development early in life.

But if we can swap out even a few of those influences, we just might be able to make life a little easier for those who need it.

This research was published in Scientific Reports.

https://www.sciencealert.com/autism-severity-cut-in-half-in-kids-who-underwent-radical-faecal-transplant-therapy

By Carl Zimmer

In 2014 John Cryan, a professor at University College Cork in Ireland, attended a meeting in California about Alzheimer’s disease. He wasn’t an expert on dementia. Instead, he studied the microbiome, the trillions of microbes inside the healthy human body.

Dr. Cryan and other scientists were beginning to find hints that these microbes could influence the brain and behavior. Perhaps, he told the scientific gathering, the microbiome has a role in the development of Alzheimer’s disease.

The idea was not well received. “I’ve never given a talk to so many people who didn’t believe what I was saying,” Dr. Cryan recalled.

A lot has changed since then: Research continues to turn up remarkable links between the microbiome and the brain. Scientists are finding evidence that microbiome may play a role not just in Alzheimer’s disease, but Parkinson’s disease, depression, schizophrenia, autism and other conditions.

For some neuroscientists, new studies have changed the way they think about the brain.

One of the skeptics at that Alzheimer’s meeting was Sangram Sisodia, a neurobiologist at the University of Chicago. He wasn’t swayed by Dr. Cryan’s talk, but later he decided to put the idea to a simple test.

“It was just on a lark,” said Dr. Sisodia. “We had no idea how it would turn out.”

He and his colleagues gave antibiotics to mice prone to develop a version of Alzheimer’s disease, in order to kill off much of the gut bacteria in the mice. Later, when the scientists inspected the animals’ brains, they found far fewer of the protein clumps linked to dementia.

Just a little disruption of the microbiome was enough to produce this effect. Young mice given antibiotics for a week had fewer clumps in their brains when they grew old, too.

“I never imagined it would be such a striking result,” Dr. Sisodia said. “For someone with a background in molecular biology and neuroscience, this is like going into outer space.”

Following a string of similar experiments, he now suspects that just a few species in the gut — perhaps even one — influence the course of Alzheimer’s disease, perhaps by releasing chemical that alters how immune cells work in the brain.

He hasn’t found those microbes, let alone that chemical. But “there’s something’s in there,” he said. “And we have to figure out what it is.”

‘It was considered crazy’

Scientists have long known that microbes live inside us. In 1683, the Dutch scientist Antonie van Leeuwenhoek put plaque from his teeth under a microscope and discovered tiny creatures swimming about.

But the microbiome has stubbornly resisted scientific discovery. For generations, microbiologists only studied the species that they could grow in the lab. Most of our interior occupants can’t survive in petri dishes.

In the early 2000s, however, the science of the microbiome took a sudden leap forward when researchers figured out how to sequence DNA from these microbes. Researchers initially used this new technology to examine how the microbiome influences parts of our bodies rife with bacteria, such as the gut and the skin.

Few of them gave much thought to the brain — there didn’t seem to be much point. The brain is shielded from microbial invasion by the so-called blood-brain barrier. Normally, only small molecules pass through.

“As recently as 2011, it was considered crazy to look for associations between the microbiome and behavior,” said Rob Knight, a microbiologist at the University of California, San Diego.

He and his colleagues discovered some of the earliest hints of these links. Investigators took stool from mice with a genetic mutation that caused them to eat a lot and put on weight. They transferred the stool to mice that had been raised germ-free — that is, entirely without gut microbiomes — since birth.

After receiving this so-called fecal transplant, the germ-free mice got hungry, too, and put on weight.

Altering appetite isn’t the only thing that the microbiome can do to the brain, it turns out. Dr. Cryan and his colleagues, for example, have found that mice without microbiomes become loners, preferring to stay away from fellow rodents.

The scientists eventually discovered changes in the brains of these antisocial mice. One region, called the amygdala, is important for processing social emotions. In germ-free mice, the neurons in the amygdala make unusual sets of proteins, changing the connections they make with other cells.

Studies of humans revealed some surprising patterns, too. Children with autism have unusual patterns of microbial species in their stool. Differences in the gut bacteria of people with a host of other brain-based conditions also have been reported.

But none of these associations proves cause and effect. Finding an unusual microbiome in people with Alzheimer’s doesn’t mean that the bacteria drive the disease. It could be the reverse: People with Alzheimer’s disease often change their eating habits, for example, and that switch might favor different species of gut microbes.

Fecal transplants can help pin down these links. In his research on Alzheimer’s, Dr. Sisodia and his colleagues transferred stool from ordinary mice into the mice they had treated with antibiotics. Once their microbiomes were restored, the antibiotic-treated mice started developing protein clumps again.

“We’re extremely confident that it’s the bacteria that’s driving this,” he said. Other researchers have taken these experiments a step further by using human fecal transplants.

If you hold a mouse by its tail, it normally wriggles in an effort to escape. If you give it a fecal transplant from humans with major depression, you get a completely different result: The mice give up sooner, simply hanging motionless.

As intriguing as this sort of research can be, it has a major limitation. Because researchers are transferring hundreds of bacterial species at once, the experiments can’t reveal which in particular are responsible for changing the brain.

Now researchers are pinpointing individual strains that seem to have an effect.

To study autism, Dr. Mauro Costa-Mattioli and his colleagues at the Baylor College of Medicine in Houston investigated different kinds of mice, each of which display some symptoms of autism. A mutation in a gene called SHANK3 can cause mice to groom themselves repetitively and avoid contact with other mice, for example.

In another mouse strain, Dr. Costa-Mattioli found that feeding mothers a high-fat diet makes it more likely their pups will behave this way.

bee-banner-1800x720-x

by IRIS KULBATSKI

Consuming a mixture of sugar syrup and glyphosate, the active ingredient in Monsanto’s Roundup herbicide, alters honey bees’ microbiomes, and these changes increased mortality among insects exposed to pathogenic bacteria, according to a study published yesterday (September 24) in PNAS.

Glyphosate is the most commonly used herbicide worldwide. It acts by blocking a key plant enzyme used in the production of amino acids. Researchers are divided on whether the chemical is safe to animals at the levels it is usually used as a herbicide. However, some bacteria are known to produce this enzyme, and the new study demonstrates what some researchers have suspected: glyphosate may harm animals indirectly by killing their resident microbes.

Nancy Moran of the University of Texas at Austin and colleagues found that glyphosate consumption can lower the levels of the common bee symbiont Snodgrassella alvi by up to five times in the guts of honey bees, and high levels of the herbicide thwarted growth of S. alvi in vitro. Moreover, bees were more susceptible to infection by Serratia marcescens, a bacterium commonly present at low levels in beehives, after drinking the glyphosate–sugar water cocktail: only 12 percent of the insects survived, compared with 47 percent of infected bees that had not been fed glyphosate.

Given these findings, more research is warranted to determine whether the proposed mechanism of honey bee morbidity contributes significantly to issues of colony collapse and overall rates of honey bee decline worldwide, University of Illinois bee geneticist Gene Robinson tells Science.

Moreover, the current study raises the possibility that glyphosate may alter the gut microbiome of other animals, including humans, Moran tells Science.

https://www.the-scientist.com/news-opinion/herbicide-may-harm-microbiome-of-bees-64860?utm_campaign=TS_DAILY%20NEWSLETTER_2018&utm_source=hs_email&utm_medium=email&utm_content=66214269&_hsenc=p2ANqtz–RVJMklVdDEAWS-ddB7O5kVzSQTWCLWqUOnn8jMfmpot3jBytURnj14l3Nx2fPlFTeNO-ZlmSqqln8Wjtd9SqOUpzqTQ&_hsmi=66214269

webp-net-resizeimage-14--x

by SUKANYA CHARUCHANDRA

Previous research has shown that the gut-brain connection, which refers to signaling between the digestive and the central nervous systems, is based on the transport of hormones, but a study published today (September 21) in Science suggests there may be a more direct link—the vagus nerve.

This research presents “a new set of pathways that use gut cells to rapidly communicate with . . . the brain stem,” Daniel Drucker, who studies gut disorders at the Lunenfeld-Tanenbaum Research Institute in Toronto, Canada, and was not involved with the project, tells Science.

Building on an earlier study in which the team found that gut cells had synapses, the researchers injected a rabies virus, expressing green fluorescence, into the stomachs of mice and watched it travel speedily from the intestines to the rodents’ brainstems.

When they grew sensory gut cells together with neurons from the vagus nerve, the neurons moved across the dish to form synapses with the gut cells and began electrically coupling with them. Adding sugar to the dish sped up the rate of signaling between the gut and brain cells, a finding that suggests glutamate, a neurotransmitter involved in sensing taste, may be key to the process. Blocking glutamate secretion in gut cells brought these signals to a grinding halt.

“We think these findings are going to be the biological basis of a new sense,” coauthor Diego Bohórquez, an assistant professor of medicine at Duke University School of Medicine, says in a statement. “One that serves as the entry point for how the brain knows when the stomach is full of food and calories. It brings legitimacy to idea of the ‘gut feeling’ as a sixth sense.”

https://www.the-scientist.com/news-opinion/the-gut-of-mice-communicates-with-the-brain-through-the-vagus-nerve-64846?utm_campaign=TS_DAILY%20NEWSLETTER_2018&utm_source=hs_email&utm_medium=email&utm_content=66141129&_hsenc=p2ANqtz–EaFM3BB6i_l04LL2zbvjlEHCWVwrSrks2D9Aksml-wGa9f88gfOwPhtiPCXEMJRqzu6WG53_vzEvHht0oAGylLgMANQ&_hsmi=66141129

microbial-activity-in-the-mouth-may-help-identify-autism-in-children

Weight gain trajectories in early childhood are related to the composition of oral bacteria of two-year-old children, suggesting that this understudied aspect of a child’s microbiota — the collection of microorganisms, including beneficial bacteria, residing in the mouth — could serve as an early indicator for childhood obesity. A study describing the results appears September 19 in the journal Scientific Reports.

“One in three children in the United States is overweight or obese,” said Kateryna Makova, Pentz Professor of Biology and senior author of the paper. “If we can find early indicators of obesity in young children, we can help parents and physicians take preventive measures.”

The study is part of a larger project with researchers and clinicians at the Penn State Milton S. Hershey Medical Center called INSIGHT, led by Ian Paul, professor of pediatrics at the Medical Center, and Leann Birch, professor of foods and nutrition at the University of Georgia. The INSIGHT trial includes nearly 300 children and tests whether a responsive parenting intervention during a child’s early life can prevent the development of obesity. It is also designed to identify biological and social risk factors for obesity.

“In this study, we show that a child’s oral microbiota at two years of age is related to their weight gain over their first two years after birth,” said Makova.

The human digestive tract is filled with a diverse array of microorganisms, including beneficial bacteria, that help ensure proper digestion and support the immune system. This “microbiota” shifts as a person’s diet changes and can vary greatly among individuals. Variation in gut microbiota has been linked to obesity in some adults and adolescents, but the potential relationship between oral microbiota and weight gain in children had not been explored prior to this study.

“The oral microbiota is usually studied in relation to periodontal disease, and periodontal disease has in some cases been linked to obesity,” said Sarah Craig, a postdoctoral scholar in biology at Penn State and first author of the paper. “Here, we explored any potential direct associations between the oral microbiota and child weight gain. Rather than simply noting whether a child was overweight at the age of two, we used growth curves from their first two years after birth, which provides a more complete picture of how the child is growing. This approach is highly innovative for a study of this kind, and gives greater statistical power to detect relationships.”

Among 226 children from central Pennsylvania, the oral microbiota of those with rapid infant weight gain — a strong risk factor for childhood obesity — was less diverse, meaning it contained fewer groups of bacteria. These children also had a higher ratio of Firmicutes to Bacteroidetes, two of the most common bacteria groups found in the human microbiota.

“A healthy person usually has a lot of different bacteria within their gut microbiota,” said Craig. “This high diversity helps protect against inflammation or harmful bacteria and is important for the stability of digestion in the face of changes to diet or environment. There’s also a certain balance of these two common bacteria groups, Firmicutes and Bacteroidetes, that tends to work best under normal healthy conditions, and disruptions to that balance could lead to dysregulation in digestion.”

Lower diversity and higher Firmicutes to Bacteroidetes (F:B) ratio in gut microbiota are sometimes observed as a characteristic of adults and adolescents with obesity. However, the researchers did not see a relationship of weight gain with either of these measures in gut microbiota of two-year-olds, suggesting that the gut microbiota may not be completely established at two years of age and may still be undergoing many changes.

“There are usually dramatic changes to an individual’s microbiota as they develop during early childhood,” said Makova. “Our results suggest that signatures of obesity may be established earlier in oral microbiota than in gut microbiota. If we can confirm this in other groups of children outside of Pennsylvania, we may be able to develop a test of oral microbiota that could be used in clinical care to identify children who are at risk for developing obesity. This is particularly exciting because oral samples are easier to obtain than those from the gut, which require fecal samples.”

Interestingly, weight gain in children was also related to diversity of their mother’s oral microbiota. This could reflect a genetic predisposition of the mother and child to having a similar microbiota, or the mother and child having a similar diet and environment.

“It could be a simple explanation like a shared diet or genetics, but it might also be related to obesity,” said Makova. “We don’t know for sure yet, but if there is an oral microbiome signature linked to the dynamics of weight gain in early childhood, there is a particular urgency to understand it. Now we are using additional techniques to look at specific species of bacteria–rather than larger taxonomic groups of bacteria–in both the mothers and children to see whether specific bacteria species influence weight gain and the risk of obesity.”

In addition to Makova, Craig, Paul, and Birch, the research team includes Jennifer Savage, Michele Marini, Jennifer Stokes, Anton Nekrutenko, Matthew Reimherr, and Francesca Chiaromonte from Penn State, Daniel Blankenberg from the Cleveland Clinic, and Alice Carla Luisa Parodi from Politecnico di Milano. INSIGHT (Intervention Nurses Start Infants Growing on Healthy Trajectories) is coordinated through the Penn State Milton S. Hershey Medical Center.

This work is supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); the Penn State Eberly College of Science; the Penn State Institute for Cyberscience; the National Center for Research Resources and the National Center for Advancing Translational Sciences of the National Institutes of Health (NIH); and the Pennsylvania Department of Health using Tobacco CURE funds.

http://science.psu.edu/news-and-events/2018-news/Makova9-2018

bacteria-crop750
Listeria bacteria transport electrons through their cell wall into the environment as tiny currents, assisted by ubiquitous flavin molecules (yellow dots). (Amy Cao graphic, copyright UC Berkeley)

By Robert Sanders

While bacteria that produce electricity have been found in exotic environments like mines and the bottoms of lakes, scientists have missed a source closer to home: the human gut.

UC Berkeley scientists discovered that a common diarrhea-causing bacterium, Listeria monocytogenes, produces electricity using an entirely different technique from known electrogenic bacteria, and that hundreds of other bacterial species use this same process.

Many of these sparking bacteria are part of the human gut microbiome, and many, like the bug that causes the food-borne illness listeriosis, which can also cause miscarriages, are pathogenic. The bacteria that cause gangrene (Clostridium perfringens) and hospital-acquired infections (Enterococcus faecalis) and some disease-causing streptococcus bacteria also produce electricity. Other electrogenic bacteria, like Lactobacilli, are important in fermenting yogurt, and many are probiotics.

“The fact that so many bugs that interact with humans, either as pathogens or in probiotics or in our microbiota or involved in fermentation of human products, are electrogenic — that had been missed before,” said Dan Portnoy, a UC Berkeley professor of molecular and cell biology and of plant and microbial biology. “It could tell us a lot about how these bacteria infect us or help us have a healthy gut.”

The discovery will be good news for those currently trying to create living batteries from microbes. Such “green” bioenergetic technologies could, for example, generate electricity from bacteria in waste treatment plants.

The research will be posted online Sept. 12 in advance of Oct. 4 print publication in the journal Nature.

Breathing metal

Bacteria generate electricity for the same reason we breathe oxygen: to remove electrons produced during metabolism and support energy production. Whereas animals and plants transfer their electrons to oxygen inside the mitochondria of every cell, bacteria in environments with no oxygen — including our gut, but also alcohol and cheese fermentation vats and acidic mines — have to find another electron acceptor. In geologic environments, that has often been a mineral — iron or manganese, for example — outside the cell. In some sense, these bacteria “breathe” iron or manganese.

microbebattery611
A microbial battery made with newly discovered electrogenic bacteria. Electrodes (CE, WE) are placed in jars full of bacteria, producing up to half a millivolt of electricity. Ajo-Franklin photo.

Transferring electrons out of the cell to a mineral requires a cascade of special chemical reactions, the so-called extracellular electron transfer chain, which carries the electrons as a tiny electrical current. Some scientists have tapped that chain to make a battery: stick an electrode in a flask of these bacteria and you can generate electricity.

The newly discovered extracellular electron transfer system is actually simpler than the already known transfer chain, and seems to be used by bacteria only when necessary, perhaps when oxygen levels are low. So far, this simpler electron transfer chain has been found in bacteria with a single cell wall — microbes classified as gram-positive bacteria — that live in an environment with lots of flavin, which are derivatives of vitamin B2.

“It seems that the cell structure of these bacteria and the vitamin-rich ecological niche that they occupy makes it significantly easier and more cost effective to transfer electrons out of the cell,” said first author Sam Light, a postdoctoral fellow. “Thus, we think that the conventionally studied mineral-respiring bacteria are using extracellular electron transfer because it is crucial for survival, whereas these newly identified bacteria are using it because it is ‘easy.’”

To see how robust this system is, Light teamed up with Caroline Ajo-Franklin from Lawrence Berkeley National Laboratory, who explores the interactions between living microbes and inorganic materials for possible applications in carbon capture and sequestration and bio-solar energy generation.

She used an electrode to measure the electric current that streams from the bacteria — up to 500 microamps — confirming that it is indeed electrogenic. In fact, they make about as much electricity — some 100,000 electrons per second per cell — as known electrogenic bacteria.

Light is particularly intrigued by the presence of this system in Lactobacillus, bacteria crucial to the production of cheese, yogurt and sauerkraut. Perhaps, he suggests, electron transport plays a role in the taste of cheese and sauerkraut.

“This is a whole big part of the physiology of bacteria that people didn’t realize existed, and that could be potentially manipulated,” he said.

Light and Portnoy have many more questions about how and why these bacteria developed such a unique system. Simplicity — it’s easier to transfer electrons through one cell wall rather than through two — and opportunity — taking advantage of ubiquitous flavin molecules to get rid of electrons – appear to have enabled these bacteria to find a way to survive in both oxygen-rich and oxygen-poor environments.

Other co-authors are Lin Su and Jose A. Cornejo of Berkeley Lab and Rafael Rivera-Lugo, Alexander Louie and Anthony T. Iavarone of UC Berkeley. The research was funded by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health and the Office of Naval Research.

http://news.berkeley.edu/2018/09/12/gut-bacterias-shocking-secret-they-produce-electricity/