disorders of the nervous system, including Guillain-Barr syndrome, MS and acute disseminated encephalomyelitis. This study may give us a foothold in understanding all of these disorders and how they are linked together. The benefit is, therefore, not only to those who are paralyzed by TM, but to those who have disabilities due to a variety of autoimmune disorders. We are actively using these findings to aid in developing future diagnostic, prognostic and therapeutic advancements," said Kerr, director of the Johns Hopkins Transverse Myelitis Center, the only center devoted to TM in the world.
Researchers analyzed 42 inflammatory proteins in the cerebrospinal fluid of both TM and healthy patients. They found that IL-6 was consistently elevated in TM patients' spinal fluid. Further, the level of IL-6 directly correlated with the severity of paralysis.
Using cell culture and animal studies, the researchers confirmed that elevated IL-6 levels were directly injurious to the spinal cord. They showed that spinal fluid from TM patients induced death of spinal cord cells when cultured in a dish and that IL-6, when infused in adult rats, induced paralysis. Under the microscope, tissue from IL-6-infused rats showed demyelination and injury of axons, pathology that was nearly identical to that seen in human patients with TM.
Kerr and Kaplin also deduced that the reason IL-6 elevations injure only the spinal cord and not other regions of the nervous system was because distinct regions of the nervous system have different responses to IL-6. They concluded that these different types of responses might be a part of why different autoimmune disorders of the nervous system affect distinct regions and cause distinct symptoms.
"When we started, we knew nothing about the bad players in this drama in the spinal cord of CNS autoimmune diseases - it was a classic murder mystery and we set out together to find out 'who done it'," said Kaplin. "We've answered w
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Contact: Eric Vohr
evohr1@jhmi.edu
410-955-8665
Johns Hopkins Medical Institutions
23-Sep-2005
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