Exercise and gut flora diversity are positively correlated

Being physically fit appears to be associated with a greater diversity of gut bugs, researchers found.

In a case-control study, Irish athletes had a far wider range of intestinal microbes than did matched controls who weren't athletes, Fergus Shanahan, MD, of the University College Cork in Ireland, and colleagues reported online in Gut.

"Exercise seems to be another important factor in the relationship between the microbiota, host immunity, and host metabolism, with diet playing an important role," they wrote.

There's been much attention surrounding gut microbiota and its relationship with obesity and metabolism, but few have looked specifically at the effects of exercise on these gut microbes.

Shanahan and colleagues looked at 40 professional athletes from an international rugby team while they participated in pre-season camp -- a regulated environment -- and compared them with healthy male controls from the Cork region of Ireland.

They found that athletes and controls differed with respect to plasma creatinine kinase, a marker of extreme exercise, and inflammatory and metabolic markers. Athletes had less inflammation and better metabolism than did controls, they reported.

Athletes also had a far higher diversity of gut bugs -- 22 phyla, 68 families, and 113 genera compared with just 11 phyla, 33 families and 65 genera for controls with a low body mass index (BMI), and 9 phyla, 33 families and 61 genera for controls with a high BMI.

Athletes also consumed far more protein than controls, with protein accounting for 22% of their total energy intake compared with 16% of energy intake for low-BMI controls and 15% for high-BMI controls.

This high protein intake, as well as high levels of creatinine kinase, positively correlated with bacterial diversity, suggesting that both diet and exercise are drivers of biodiversity in the gut, Shanahan and colleagues wrote.

The results provide evidence that exercise has a beneficial effect on gut microbiota diversity, they concluded, but it also indicates that the relationship is complex since it's also tied to dietary extremes -- which is why further investigation is needed into the relationship, with a particular need for intervention-based studies to tease it apart.

In an accompanying editorial, Georgina Hold, MD, of the University of Aberdeen in Scotland, noted that the article is the first to report that exercise increases gut microbe diversity and that it "highlights that exercise is another important factor in the complex relationship among the host, host immunity, and the microbiota."

She added that future studies examining the impact of exercise and the nutritional value of foods in terms of relevance to gut bacteria are essential: "Developing new ways to manipulate the beneficial properties of our microbiota by finding ways to integrate health-promoting properties into modern living should be the goal."

Viruses in gut confer antibiotic resistance to bacteria

http://www.vetscite.org/publish/items/008045/index.html

25 June 2013

Potential new target to thwart antibiotic resistance: Viruses in gut confer antibiotic resistance to bacteria


Bacteria in the gut that are under attack by antibiotics have allies no one had anticipated, a team of Wyss Institute scientists has found. Gut viruses that usually commandeer the bacteria, it turns out, enable them to survive the antibiotic onslaught, most likely by handing them genes that help them withstand the drug. What's more, the gut viruses, called bacteriophage or simply phage, deliver genes that help the bacteria to survive not just the antibiotic they've been exposed to, but other types of antibiotics as well, the scientists reported online June 9 in Nature. That suggests that phages in the gut may be partly responsible for the emergence of dangerous superbugs that withstand multiple antibiotics, and that drug targeting of phages could offer a potential new path to mitigate development of antibiotic resistance. "The results mean that the antibiotic-resistance situation is even more troubling than we thought," said senior author Jim Collins, Ph.D., a pioneer of synthetic biology and Core Faculty member at the Wyss Institute for Biologically Inspired Engineering, who is also the William F. Warren Distinguished Professor at Boston University, where he leads the Center of Synthetic Biology.

Today disease-causing bacteria have adapted to antibiotics faster than scientists can generate new drugs to kill them, creating a serious global public-health threat. Patients who are hospitalized with serious bacterial infections tend to have longer, more expensive hospital stays, and they are twice as likely to die as those infected with antibiotic-susceptible bacteria, according to the World Health Organization. In addition, because first-line drugs fail more often than before, more expensive therapies must be used, raising health-care costs. In the past, Collins and other scientists have probed the ways gut bacteria adapt to antibiotics, but they've focused on the bacteria themselves. But Collins and Sheetal Modi, Ph.D., the lead author of the study and a postdoctoral fellow in Collins' laboratory and at the Wyss Institute, knew that phage were also abundant in the gut, and that they were adept at ferrying genes from one bacterium to another. The researchers wondered whether treating mice with antibiotics led phage in the gut to pick up more drug-resistance genes, and if so, whether that made gut bacteria stronger. They gave mice either ciprofloxacin or ampicillin -- two commonly prescribed antibiotics. After eight weeks, they harvested all the viruses in the mice's feces, and identified the viral genes present by comparing them with a large database of known genes. They found that the phages from antibiotic-treated mice carried significantly higher numbers of bacterial drug-resistance genes than they would have carried by chance. What's more, phage from ampicillin-treated mice carried more genes that help bacteria fight off ampicillin and related penicillin-like drugs, while phage from ciprofloxacin-treated mice carried more genes that help them fight off ciprofloxacin and related drugs. "When we treat mice with certain classes of drugs, we see enrichment of resistance genes to those drug classes," Modi said. The phage did more than harbor drug-resistance genes. They could also transfer them back to gut bacteria -- a necessary step in conferring drug resistance. The researchers demonstrated this by isolating phage from either antibiotic-treated mice or untreated mice, then adding those phage to gut bacteria from untreated mice.

Phage from ampicillin-treated mice tripled the amount of ampicillin resistance, while phage from ciprofloxacin-treated mice doubled the amount of ciprofloxacin resistance. That was bad enough, but the scientists also found signs that the phage could do yet more to foster antibiotic resistance. That's because gut phage from mice treated with one drug carried high levels of genes that confer resistance to different drugs, which means that the phage could serve as backup when bacteria must find ways to withstand a variety of antibiotics. "With antibiotic treatment, the microbiome has a means to protect itself by expanding the antibiotic resistance reservoir, enabling bugs to come back to be potentially stronger and more resistant than before," Collins said. "Antibiotic resistance is as pressing a global health problem as they come, and to fight it, it's critical to understand it," said Don Ingber, M.D., Ph.D., Wyss Institute Founding Director. "Jim's novel findings offer a previously unknown way to approach this problem -- by targeting the phage that live in our intestine, rather than the pathogens themselves."

Science Daily
June 25, 2013

Original web page at Science Daily