It isn’t just the bacteria in our gut that play an important role in keeping us healthy — yeasts and other fungi that live there are also key parts of the equation. But how exactly all these microbes interact with our bodies isn’t well understood. In new research involving mice, researchers found that a healthy immune system corrals fungi from turning into their more harmful form. Without that mitigation, the fungi may then contribute to chronic gut conditions like Crohn’s disease.
The connection between gut bacteria and our overall health has been well studied in recent years. And while many of the specifics of this relationship are still unknown, it’s clear that a balanced microbiome with the right mix of bacteria helps maintain many of our regular bodily functions; conversely, the wrong mix of bacteria might help cause or signal the emergence of illness. But bacteria are only one type of microbe, and there’s been less work studying the many viruses and fungi that inhabit our body.
This new research was conducted by scientists from the University of Utah Health, who were curious if fungi were relevant to the development of inflammatory bowel disease (IBD), which includes Crohn’s. IBD is a complicated disorder, thought to have several contributing factors, including genetics. But recent research has suggested that certain species of fungi and yeast (the single celled version of fungi) could be one of these risk factors, including a common fungi in our gut called Candida albicans.
In experiments with mice, the team noticed that a functioning immune system seemed to interact with C. albicans. The yeast has the uncanny ability to switch between different forms of growth. It can remain a ball-like single-celled organism, or it can turn into a multicellular form, decked out with hyphae, a common branch-like structure found in most other fungi, that allows it to invade the tissues of our body to keep growing. The team found evidence that antibodies specific to C. albicans didn’t outright try to kill it — instead, they kept the yeast from turning into this more invasive form. But once the yeast was allowed to grow unfettered, the mice became sick with IBD-like symptoms, which can include diarrhoea, intense cramps, and weight loss.
The study’s results, published in Nature on Tuesday, not only point to a possible instigator of IBD symptoms but also suggest that there’s a complicated relationship between us and fungi like C. albicans, the researchers say. The yeast is a common source of opportunistic infection, but keeping it around in some capacity and neutered may be important to a healthy gut (it also allows the yeast to survive undetected, likely for longer than it would if it caused a full blown infection).
“The immune system is constraining Candida to its least pathogenic form,” said lead author Kyla Ost, a postdoctoral researcher at the University of Utah Health, in a statement. “This is showing us that the communication between host and microbe can be friendly, as opposed to antagonistic, in order to benefit both.”
Research elsewhere has pointed to other species of fungi that could be a contributing factor to IBD, though not necessarily as the original source of a person’s illness. It’s likely that many cases of IBD will be linked to multiple factors working together (or becoming dysfunctional) in tandem. But if this research does continue to show promise, specifically in people, it may lead to new avenues of treatment. In other experiments, Ost and her team found that mice given an experimental vaccine meant to prevent vaginal yeast infections from C. albicans also appeared to be better protected from developing IBD-like symptoms.
The team plans to keep studying whether vaccines could help alleviate IBD symptoms, which tend to stay dormant then flare up. They also hope to find similar ways to nudge a dysfunctional gut microbiome back into balance.
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