Science Human intestinal bacteria can cause multiple sclerosis

Science Human intestinal bacteria can cause multiple sclerosis / Health News
New research findings: Natural intestinal flora can trigger multiple sclerosis
Multiple sclerosis (MS) is the most common inflammatory disease of the central nervous system. The exact causes of the disease are so far largely unclear. A research team has now found evidence that human gut bacteria can trigger MS.


Causes of Multiple Sclerosis
According to experts, multiple sclerosis (MS) is the most common inflammatory disease of the central nervous system. The exact causes of the disease are not yet clear. Hereditary factors and environmental factors are believed to lead to a malfunction of the immune system. German researchers also reported that specific coagulation factors could be possible triggers of MS. And an international team of scientists has now found evidence that human intestinal bacteria can trigger multiple sclerosis.

The exact causes of multiple sclerosis are still unclear. Researchers have now found evidence that human gut bacteria can trigger MS. (Photo: Zerbor / fotolia.com)

Incurable disease
Despite intensive research, the disease is still considered incurable. Nevertheless, researchers are cautiously optimistic about the future. Thanks to new drugs, MS is becoming increasingly manageable.

In addition, certain plant peptides can stop the MS course, as scientists found.

According to research, with proper nutrition you can slow down multiple sclerosis.

And experts from various research institutions reported in the journal "Journal of Neurology, Neurosurgery and Psychiatry" that increased coffee consumption can reduce MS risk by up to 30 percent.

Also in the investigation of the cause of the disease, further successes have now been achieved.

Nerve stimuli are no longer passed on correctly
In autoimmune diseases such as multiple sclerosis, misdirected cells of the immune system attack the body's own cells in the brain and spinal cord.

The attack triggered by autoaggressive T cells damages the affected nerve cells and leads to the degradation of their cladding layer. Cells die and nerve stimuli are no longer transmitted correctly.

Everybody has potentially autoaggressive T cells, but the cells are usually in a "sleep state" for life. In some people, however, the pathogenic potential of these cells is awakened - it comes to the onset of MS.

The reason for this activation scientists suspect in a combination of genetics and environmental factors.

"We now know more than 200 genes that make humans susceptible to MS," explains Hartmut Wekerle from the Max Planck Institute for Neurobiology in a statement.

"However, in order for it to break out, it needs a trigger that was previously sought in the environment of infections."

Trigger in the natural intestinal flora
Years ago, the expert and colleagues found out that this trigger is probably to be found in the natural intestinal flora.

Now they were able to show that microorganisms in the gut of genetically modified, autoimmune mice were able to activate T cells, after which the animals developed an inflammation in the brain similar to human disease.

After it has been shown in animal experiments that intestinal bacteria can trigger multiple sclerosis, a large number of studies investigated and compared the composition of the intestinal flora of healthy people with MS.

"The genetic diversity of these people and their intestinal flora, however, made it very difficult to draw concrete conclusions from the results," said Wekerle.

"In addition, the presence of a particular microorganism in MS patients does not say anything about whether it actually takes on a role in disease development. This can only be clarified with the help of animal experiments. "

The researchers avoided these difficulties in a large collaborative project in which they closely linked clinical investigations and basic research.

Only one twin is affected
The basic idea of ​​the cooperation project was the comparison of the intestinal flora of identical pairs of twins. In rare cases, MS patients have identical twin siblings, with only one twin suffering from multiple sclerosis in most cases, while the other is healthy.

This is an indication that other than genetic factors are effective in the development of MS.

As part of the cooperation project, more than 50 identical twins were recruited throughout Germany, with one twin suffering from multiple sclerosis.

Since each pair of twins is genetically identical, this should reveal MS-relevant differences in the intestinal flora. Because the influence of human genes on the intestinal flora can be neglected in the pairwise comparisons.

Functional role in T cell activation
When comparing the intestinal flora of the twins showed some interesting, albeit subtle differences.

"It got really exciting, however, when we inoculated the germ-free, genetically modified mice with the respective human microbiome," says Guru Krishnamoorthy of the Max Planck Institute of Biochemistry.

Animals that received gut flora samples from MS-infected twins were almost 100 percent ill with MS-like brain inflammation.

The investigations confirmed for the first time that constituents of the intestinal flora of MS patients play a functional role in T-cell activation and thus can be a trigger for multiple sclerosis in humans.

Narrow down the candidate microorganisms
"Now it is important to further delineate and investigate the microorganisms in question", says Wekerle.

However, the doctor points out that the examinations will certainly take off over the years and that it is still unclear whether and which diagnostic and therapeutic procedures can emerge from them.

Of the currently discussed in the media "fecal grafting" (stool transplantation) of healthy people on MS patients as "quick help", he holds nothing: "because you never know exactly what's in it!"

In addition to the experts from the Max Planck Institutes for Neurobiology and Biochemistry in Martinsried near Munich, researchers from the Ludwig-Maximilians-University Munich, the Max Planck Institute of Immunobiology and Epigenetics in Freiburg and the Universities of California (San Francisco) and Münster participated in the scientific work. (Ad)