Posts Tagged ‘microbiome’

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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

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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

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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

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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.

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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/

Consumption of dietary fiber can prevent obesity, metabolic syndrome and adverse changes in the intestine by promoting growth of “good” bacteria in the colon, according to a study led by Georgia State University.

The researchers found enriching the diet of mice with the fermentable fiber inulin prevented metabolic syndrome that is induced by a high-fat diet, and they identified specifically how this occurs in the body. Metabolic syndrome is a cluster of conditions closely linked to obesity that includes increased blood pressure, high blood sugar, excess body fat around the waist and abnormal cholesterol or triglyceride levels. When these conditions occur together, they increase a person’s risk of heart disease, stroke and diabetes.

Obesity and metabolic syndrome are associated with alterations in gut microbiota, the microorganism population that lives in the intestine. Modern changes in dietary habits, particularly the consumption of processed foods lacking fiber, are believed to affect microbiota and contribute to the increase of chronic inflammatory disease, including metabolic syndrome. Studies have found a high-fat diet destroys gut microbiota, reduces the production of epithelial cells lining the intestine and causes gut bacteria to invade intestinal epithelial cells.

This study found the fermentable fiber inulin restored gut health and protected mice against metabolic syndrome induced by a high-fat diet by restoring gut microbiota levels, increasing the production of intestinal epithelial cells and restoring expression of the protein interleukin-22 (IL-22), which prevented gut microbiota from invading epithelial cells. The findings are published in the journal Cell Host & Microbe.

“We found that manipulating dietary fiber content, particularly by adding fermentable fiber, guards against metabolic syndrome,” said Dr. Andrew Gewirtz, professor in the Institute for Biomedical Sciences at Georgia State. “This study revealed the specific mechanism used to restore gut health and suppress obesity and metabolic syndrome is the induction of IL-22 expression. These results contribute to the understanding of the mechanisms that underlie diet-induced obesity and offer insight into how fermentable fibers might promote better health.”

For four weeks, the researchers fed mice either a grain-based rodent chow, a high-fat diet (high fat and low fiber content with 5 percent cellulose as a source of fiber) or a high-fat diet supplemented with fiber (either fermentable inulin fiber or insoluble cellulose fiber). The high-fat diet is linked to an increase in obesity and conditions associated with metabolic syndrome.

They discovered a diet supplemented with inulin reduced weight gain and noticeably reduced obesity induced by a high-fat diet, which was accompanied by a reduction in the size of fat cells. Dietary enrichment with inulin also markedly lowered cholesterol levels and largely prevented dysglycemia (abnormal blood sugar levels). The researchers found insoluble cellulose fiber only modestly reduced obesity and dysglycemia

Supplementing the high-fat diet with inulin restored gut microbiota. However, inulin didn’t restore the microbiota levels to those of mice fed a chow diet. A distinct difference in microbiota levels remained between mice fed a high-fat diet versus those fed a chow diet. Enrichment of high-fat diets with cellulose had a mild effect on microbiota levels.

In addition, the researchers found switching mice from a grain-based chow diet to a high-fat diet resulted in a loss of colon mass, which they believe contributes to low-grade inflammation and metabolic syndrome. When they switched mice back to a chow diet, the colon mass was fully restored.

https://www.technologynetworks.com/tn/news/fiber-rich-diet-fights-off-obesity-by-altering-microbiota-296642?utm_campaign=Newsletter_TN_BreakingScienceNews&utm_source=hs_email&utm_medium=email&utm_content=60184554&_hsenc=p2ANqtz-9YDsGiTl44CBfQpgNtYgc43xBeVKpAbPZym9Lh_GzlHoEVts0rAwMhHHXIDam3Jit0D3aTqKGhCceUREgr6sZfLGMWpQ&_hsmi=60184554

By Ann Gibbons

Humans did not evolve alone. Tens of trillions of microbes have followed us on our journey from prehistoric ape, evolving with us along the way, according to a new study. But the work also finds that we’ve lost some of the ancient microbes that still inhabit our great ape cousins, which could explain some human diseases and even obesity and mental disorders.

Researchers have known for some time that humans and the other great apes harbor many types of bacteria, especially in their guts, a collection known as the microbiome. But where did these microbes come from: our ancient ancestors, or our environment? A study of fecal bacteria across all mammals suggested that the microbes are more likely to be inherited than acquired from the environment. But other studies have found that diet plays a major role in shaping the bacteria in our guts.

To solve the mystery, Andrew Moeller turned to wild apes. As part of his doctoral dissertation, the evolutionary biologist, now a postdoc at the University of California, Berkeley, studied gut bacteria isolated from fecal samples from 47 chimpanzees from Tanzania, 24 bonobos from the Democratic Republic of the Congo, 24 gorillas from Cameroon, and 16 humans from Connecticut. In these samples, he and colleagues at the University of Texas (UT), Austin, compared the DNA sequences of a single rapidly evolving gene that is common in the gut bacteria in apes, including humans. They then sorted the different DNA gene sequences into family trees.

It turns out that most of our gut microbes have been evolving with us for a long time. Moeller found that two of three major families of gut bacteria in apes and humans trace their origins to a common ancestor more than 15 million years ago, not primarily to bugs picked up from their environment. But as the different species of apes diverged from this ancestor, their gut bacteria also split into new strains, and coevolved in parallel (a process known as cospeciation) to adapt to differences in the diets, habitats, and diseases in the gastrointestinal tracts of their hosts, the team reports today in Science. Today, these microbes are finely adapted to help train our immune systems, guide the development of our intestines, and even modulate our moods and behaviors.

“It’s surprising that our gut microbes, which we could get from many sources in the environment, have actually been coevolving inside us for such a long time,” says project leader Howard Ochman, an evolutionary biologist at UT Austin.

After the ape species diverged, some also lost distinct strains of bacteria that persisted in other primates, likely another sign of adaptation in the host, the team found.

In a final experiment, the researchers probed deeper into the human microbiome. They compared the same DNA sequence they had analyzed in all of the apes, but this time between the people from Connecticut and people from Malawi. They found that the bacterial strains from these Africans diverged from those of the Americans about 1.7 million years ago, which corresponds with the earliest exodus of human ancestors out of Africa. This suggests that gut bacteria can be used to trace early human and animal migrations, Moeller says. Interestingly, the Americans lacked some of the strains of bacteria found in Malawians—and in gorillas and chimps—which fits with the general reduction in gut microbiome diversity that has been observed in people in industrialized societies, perhaps because of changes in diet and the use of antibiotics.

The work “represents a significant step in understanding human microbiota coevolutionary history,” says Justin Sonnenburg of Stanford University in Palo Alto, California, who was not involved with the research. “It elegantly shows that gut microbes are passed vertically, between generations over millions of years.” Microbiologist Martin Blaser of New York University in New York City agrees: “The path of transmission was from mom apes to baby apes for hundreds of thousands of generations at least.”

But the extinction of some strains of bacteria that persist in other apes but not humans raises a red flag for our health. “What happens if a human mom takes antibiotic when she’s pregnant? What happens if she takes it at the moment of delivery?” Blaser asks.

“We are coming to understand how fundamental our gut microbes are for health,” Sonnenburg says. “These findings have huge implications for how we should pursue understanding what a truly healthy microbiome looks like.”

http://www.sciencemag.org/news/2016/07/microbes-our-guts-have-been-us-millions-years

Thanks to Kebmodee for bringing this to the It’s Interesting community.


Once scientists grew these Staphylococcus lugdunensis bacteria in a lab dish, they were able to isolate a compound that’s lethal to another strain commonly found in the nose that can make us sick — Staphylococcus aureus.

by Carolyn Beans

With antibiotic-resistant super bugs on the rise, researchers are on an urgent hunt for other bacteria that might yield chemicals we can harness as powerful drugs. Scientists once found most of these helpful bacteria in soil, but in recent decades this go-to search location hasn’t delivered.

Now, researchers at the University of Tübingen in Germany say that to find at least one promising candidate, we need look no further than our own noses.

The scientists report Wednesday in the journal Nature that a species of bacteria inside the human nose produces a substance capable of killing a range of bacteria, including the strain of drug-resistant Staphylococcus aureus known as MRSA.

The Tübingen team is delighted with their find. “It was totally unexpected,” says study author Andreas Peschel.

The scientists already knew that S. aureus lives in the noses of about 30 percent of humans, usually without causing harm — most people never know they are carriers of the bacterium. But if the body becomes compromised (whether by surgery, physical trauma, an underlying illness or suppressed immune system) the little cache of S. aureus in the nose can suddenly launch an attack against its human host. And if the strain of bacteria is MRSA, that infection can be lethal.

The scientists wondered how 70 percent of human noses are able to avoid harboring S. aureus. They guessed it might have something to do with neighboring bacteria.

So the researchers pitted 90 different human nasal bacteria in one-on-one battles with S. aureus in the lab. Indeed, one of these bacteria — Staphylococcus lugdunensis — prevented the dangerous pathogen from growing.

They then studied the arsenal of chemicals that S. lugdunensis produces until they found one that stops S. aureus in its tracks – a new antibiotic that they named lugdunin.

Follow-up work confirmed that lugdunin can treat S. aureus skin infections in mice, and limit the spread of S. aureus in a rat’s nose.

Lugdunin may already be keeping S. aureus out of our noses. In a group of 187 hospitalized people, the same scientists found S. aureus in the noses of just 5.9 percent of people who also harbored the lugdunin-producing bacteria, but 34.7 percent of those who didn’t.

Other recent studies have shown that bacteria living in humans carry genes that have the potential to make antibiotics. The Tübingen study takes those results a step further by showing that an antibiotic produced by a bacterium in the human nose can successfully treat an animal’s infection.

“This paper is a really nice follow-up,” says Dr. Nita Salzman, a pathologist at the Medical College of Wisconsin. “It’s a sort of proof of principle that the microbiome is a good source for novel antibiotics.”

The researchers have applied for a patent for lugdunin, but say that the prototype antibiotic is still many years away from being ready to treat humans.

The really important contribution of this study is not lugdunin itself, says microbiologist Kim Lewis of Northeastern University, but rather the new approach for finding antibiotic-producing bacteria within our own bodies.

“The reason we ran out of antibiotics in the first place is because most of them came from soil bacteria and they make up 1 percent of the total [bacterial] diversity,” Lewis says.

Scientists kept searching in soil, he says, because they already had some success there and know that soil bacteria are exceptionally good at producing antibiotics.

But now it’s time to look within us. And the team in Tübingen has only just begun their hunt.

“We have started a larger screening program and we’re sure there will be many additional antibiotics that can be discovered,” says Peschel.

http://www.npr.org/sections/health-shots/2016/07/27/487529338/nose-y-bacteria-could-yield-a-new-way-to-fight-infection