The origins of multiple sclerosis apparently lie in an abnormal assault by the body's immune system against certain parts of the central nervous system, which include the brain and spinal cord.¹

Similar Proteins Targeted?
Though it hasn't been clear as to the cause of this immune system miscue, a new study from Switzerland suggests that a certain bacterium or virus may be the culprit.² These bacterial infections, the Swiss study team claims, induce a kind of self-recognition that may contribute to some autoimmune diseases such as MS and Guillain-Barre syndrome (GBS).

These organisms produce an infection that may stimulate the production of antibodies that make up the immune system, as well as immune cells known as T-cells. The theory is that the immune cells target bacterial proteins that closely resemble the body's own proteins, leading to crossreactivity with healthy tissues.

Alternative Theory
However, in the latest study, Gennaro de Libero, MD, at University Hospital in Basel, Switzerland, and his associates identified another possible mechanism. In this case, bacterial infections may promote activation of T cells that recognize special molecules present in bacteria and humans known as glycosphingolipids (gly-koh-sfin-goh-LIH-pids), or GSL. The research team showed that infection with some bacteria or even exposure to pieces of the outer wall of the bacteria results in an increase in T-cell response to these molecules.

"This stimulation may contribute to inflammatory responses during bacterial infections and may predispose individuals to autoimmune diseases," de Libero's team wrote. It's an important mechanism that leads to autoreactive T-cell activation in the immune system, and may take part in the origins of many other autoimmune diseases, de Libero explained.

The investigators theorize that although autoreactive T-cells may play a beneficial role in promoting the response to infection in the body, in the absence of infection, these T-cells might instead seek out the abundant GSL molecules found in the central nervous system, resulting in the damage to tissue in that part of the body seen in people with MS.

Another disease in which this mechanism may be found includes Guillain-Barr syndrome (GBS), "in which the anti-GSL T-cell response may be important," de Libero explained.

No Definite Conclusions Yet
Other research has focused on the possible role of disease-causing organisms as an underlying source of MS. For instance, in 2003, Spanish researchers assessed the levels of antibodies that were associated with three pathological organisms in the blood samples taken from a group of people with MS.³

The study team found "a strong association" between antibodies against human herpesvirus type 6 (anti-HHV-6), one of the many herpesviruses, and the early stages of multiple sclerosis, particularly in those with the relapsing form of the disease. Antibodies against Epstein-Barr virus were also linked with MS in these patients, the study team noted.

In a review paper on the subject,⁴ doctors at Wayne State University in Detroit reviewed previous studies that suggested a link between MS and certain bacterial or viral infections. However, they found many inconsistent observations, writing that "no conclusion is possible at this point".

1. National Multiple Sclerosis Society. What is Multiple Sclerosis? Available at: http://www.nationalmssociety.org/What%20is%20MS.asp.
2. De Libero G, Moran AP, Gober HJ et al. Bacterial infections promote T cell recognition of self-glycolipids. Immunity 2005 Jun;22(6):763-72.
3. Villoslada P, Juste C, Tintore M et al. The immune response against herpesvirus is more prominent in the early stages of MS. Neurology 2003 Jun 24;60(12):1944-8.
4. Swanborg RH, Whittum-Hudson JA, Hudson AP. Infectious agents and multiple sclerosis—are Chlamydia pneumoniae and human herpes virus 6 involved? J Neuroimmunol 2003 Mar;136(1-2):1-8.

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John Martin is a long-time health journalist and an editor for Priority Healthcare. His credits include overseeing health news coverage for the website of Fox Television's The Health Network, and articles for the New York Post and other consumer and trade publications.