The maternal gut microbiome guides neo- and postnatal immune system development, a mouse study shows.
Pregnant mice expose their unborn pups to maternal gut microbes, which can affect the development of the innate immune system after birth, according to a study published today (March 17) in Science. The results challenge the notion that a pup’s own gut microbiome drives immune system development, suggesting that the molecular metabolites of the maternal microbiota are transferred to pups during gestation. This transfer of maternally derived microbial metabolites prepares the offspring’s immune system for exposure to the large variety of microbes that eventually populate the gut.
It’s not always talked about in polite company, but your body produces a lot of gases scientists know little about.
A new smart pill, designed at Melbourne’s RMIT University, could help us learn more and may eventually assist in customising what we eat to suit our bodies.
Researchers from the Centre for Advanced Electronics and Sensors have developed the pill, which can measure intestinal gases, and they have now undertaken the first animal tests using the technology to examine the impact of fibre on the gut.
RMIT professor Kourosh Kalantar-zadeh, whose previous work has included pollution-detecting sensors, told Mashable Australia the development could tell us more about issues linked to intestinal gases, including colon cancer, irritable bowel syndrome and inflammatory bowel disease.
Since his discovery in 1991, Ötzi the “Iceman” — an intact, naturally mummified man believed to have lived in the Italian Alps approximately 5,300 years ago — has captured the international imagination and provided a tantalizing glimpse into life during the Copper Age.
Now, a new research project, which analyzed the genetic composition of bacteria in the Iceman’s stomach, is giving scientists insight into not only the Iceman’s personal life, but the history of human geography at large.
The scientists, who published their study in the journal Science on Thursday, focused on a type of common bacteria called Helicobacter pylori, or H. pylori. Found in about two thirds of the world’s population, according to the National Institutes of Health, it usually inhabits the stomach and is capable of causing infections that can lead to ulcers or even stomach cancer.
In a battle against an infection, antibiotics can bring victory over enemy germs. Yet that war-winning aid can come with significant collateral damage; microbial allies and innocents are killed off, too. Such casualties may be unavoidable in some cases, but a lot of people take antibiotics when they’re not necessary or appropriate. And the toll of antibiotics on a healthy microbiome can, in some places, be serious, a new study suggests.
In two randomized, placebo-controlled trials of healthy people, a single course of oral antibiotics altered the composition and diversity of the gut microbiome for months, and in some cases up to a year. Such shifts could clear the way for pathogens, including the deadly Clostridium difficile. Those community changes can also alter microbiome activities, including interacting with the immune system and helping with digestion. Overall, the data, published Tuesday in the journal mBio, suggests that antibiotics may have more side effects than previously thought—at least in the gut.
A strain of the dysentery-causing bacterium isolated in 1915 tells the story of a young soldier who died of the disease in the early days of World War I.
In early 1915, less than a year into the First World War, Private Ernest Cable, a 28-year-old British soldier serving in the 2nd Battalion of the East Surrey Regiment, stumbled into No. 14 Stationary Hospital in Wimereux, France. He was suffering from severe abdominal cramping and bloody diarrhea. Doctors diagnosed him with dysentery. Not long after, Cable was dead.
Nicholas Thomson, a genomicist at the Wellcome Trust Sanger Institute, first came to know of Cable’s lethal infection at a conference in October 2011. At the meeting, he met a woman named Philippa “Pippa” Bracegirdle, who worked in the archives of the UK National Collection of Type Cultures (NCTC), the oldest collection of bacterial cultures in the world. Over a drink, Bracegirdle mentioned that the collection contained an isolate of Shigella, the dysentery-causing kin of E. coli that had killed Cable. Later identified as Shigella flexneri serotype 2a, it was the first bacterial isolate deposited in NCTC’s now 5,000-sample-strong biobank.
With the 100-year anniversary of the start of “the war to end all wars” coming up in just a few years, Thomson was inspired to take a closer look at the isolate. Having studied the genetics of Shigella and other pathogens, he decided to sequence the bacterium. But as Thomson learned more from Bracegirdle about the isolate, he realized he had a rare opportunity to find out more about the patient who died from it a century ago.
During systemic infection, mice kick-start the production of a specific sugar to feed and protect the beneficial bacteria in their guts while fighting pathogenic strains.
Mice with systemic bacterial infections induce a pathway that makes a sugar called fucose readily available to feed the beneficial microbiota in the small intestine, according to a study published today (October 1) in Nature. This newly uncovered protective mechanism helps maintain the “good” bacterial populations in the gut while the animal is sick—and appears to protect against further infections.
“The most interesting aspect of this study is that the host is responding to a systemic microbial infection signal by altering glycans on intestinal epithelial cells, and this in turn increases host fitness in a microbiota-dependent manner,” saidLaurie Comstock, a microbiologist at the Brigham and Women’s Hospital in Boston who wrote an editorial accompanying the study but was not involved in the work.
In the event of systemic bacterial infection, the host will try to neutralize or kill the harmful bacteria—known as a resistance response—and mitigate the negative impacts of the infection without directly targeting the pathogens—through what’s called a tolerance response. The innate immune system is known to mediate resistance mechanisms to these infections partly by releasing the cytokine IL-22 from innate lymphoid cells. This latest study now shows that IL-22 is also responsible for a tolerance response, by controlling this newly identified fucosylation pathway in the gut in response to the infection
The pace at which bacterial groups take root in the gastrointestinal tracts of premature infants is more tied to developmental age than time since birth.
Infants start out mostly microbe-free but quickly acquire gut bacteria, which take root in three successive groups. First, Bacilli dominate. Then Gammaproteobacteria surge, followed by Clostridia. But the pace at which these bacterial groups colonize the gastrointestinal tract depends on the time since the babies were conceived, not since when they were born. And time since conception appears to have more of an influence on the infant gut microbiome than other factors, such as exposure to antibiotics, whether babies were born vaginally or by cesarean section, and if they were breastfed. These are a few of the findings from a survey of 922 fecal samples collected from 58 premature babies, published today (August 11) in PNAS.