Gut Bacteria Could Cause MS in Younger Patients


Mouse models engineered with MS-associated risk genes developed an equivalent MS condition and bowel inflammation after being exposed to an environment with bacteria present.

Suhayl Dhib-Jalbut, MD, Robert Wood Johnson

Suhayl Dhib-Jalbut, MD

Alterations to gut microbiota may be a driving factor in multiple sclerosis (MS) inflammation and progression in young patients, according to a recent study.

Mouse models engineered with MS-associated risk genes developed an equivalent MS condition and bowel inflammation after being exposed to an environment with bacteria present, researchers from the Rutgers-Robert Wood Johnson Medical School (RWJ) reported.

Though the relationship between gut microbiota alteration (gut dysbiosis) and MS has been observed previously, the discovery that the relationship could be age-dependent is novel in the study, Suhayl Dhib-Jalbut, MD, Director of the RWJ Center for Multiple Sclerosis, told MD Magazine.

“In children, MS is generally more inflammatory,” Dhib-Jalbut said. “It’s a disease of young people, and there’s a peak incidence in the second or third decade. At a younger age, bacteria is more likely to result in the disease, or exacerbate the disease and cause its progression.”

Progression and development of the animal model of MS, encephalomyelitis, was more prominent in younger mice, and was seemingly triggered by gut dysbiosis and MS-risk genes, according to the study. It’s the first documentation of identified mechanisms by which gut dysbiosis triggers immune system changes that underlie MS progression.

The results also suggest that dysbiosis may play a role in MS pathology during a particular age window.

“We found that the way bacteria influences the MS condition is through alteration of the immune system,” Dhib-Jalbut said. “One of these alterations had to do with the immunity of the gut — bacteria can get into the blood and access the brain.”

Bacteria also affected the body’s regulatory T-cells count, Dhib-Jalbut said, lessening the body’s defense against disease.

The MS-engineered mice were initially placed in a safe, germ-free environment, prior to being exposed to potential bacteria, as control. Though the pollutant exposure resulted in MS and gut inflammation, Dhib-Jalbut said there also appeared to be bacteria that worked to prevent the inflammatory disease in subjects.

As a result, researchers may be able to manipulate pollutant bacteria to limit inflammation and MS exacerbation.

“The implication is that it’s possible — by manipulating gut bacteria with medications and antibiotics, and eliminiating certain gut bacteria — we can prevent MS,” Dhib-Jalbut said. “We have to identify the bacteria components that are harmful, versus those that are beneficial, and that’s what we’re currently investigating.”

There is still a need for better understanding in the relationship between gut dysbiosis and MS, Dhib-Jalbut said. When asked whether he believes environment toxins or pollution could play a role in young people developing MS, he said such an answer could not be concluded from this study.

While Vitamin D deficiency, smoking, and obesity are among the known risk factors in early MS development and progression, there are no known conclusions regarding the environment’s role in the disease.

A 10-year study published earlier this year found that disease relapse in patients with MS may be triggered by season-dependent factors such as ambient air pollution.

Dhib-Jalbut maintained that their research will continue to focus on MS pathology — and possibly prevention — through gut bacteria.

“What we really know about is gut bacteria, and we are trying to explore that and find the harmful bacteria versus the beneficial bacteria,” Dhib-Jalbut said.

The study, "Gut dysbiosis breaks immunological tolerance toward the central nervous system during young adulthood," was published online in the journal PNAS last month.

A press release regarding the study was made available.

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