Cytokines hold promise as MS therapy

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Cytokines hold promise as MS therapy

Last Updated: 2002-06-03 16:50:49 -0400 (Reuters Health)

By Merritt McKinney

NEW YORK (Reuters Health) - Two related chemicals in the body may be

involved in preventing the nerve damage caused by the degenerative

neurological disease multiple sclerosis (MS), the results of two new studies

suggest.

The findings could lead to therapies that battle MS in a different way than

current drugs, researchers say.

In MS, the slow destruction of myelin--the thin, protective coating that

insulates nerve fibers in the brain and spine--can lead to numbness, muscle

weakness and stiffness, impaired vision and coordination problems.

A substance called ciliary neurotrophic factor (CNTF) is believed to promote

the survival of myelin-producing cells called oligodendrocytes. To find out

how CNTF affects myelin-destroying diseases such as MS, a team led by Dr.

Ralf Gold, of the Julius-Maximilians-Universitat-Wurzburg in Germany,

studied mice that lacked the gene for CNTF. They worked with mice that were

prone to develop experimental autoimmune encephalomyelitis, or EAE, a

condition that also destroys myelin and that is used by researchers to mimic

MS in mice.

The CNTF-lacking mice and a group of mice that had the CNTF gene developed

EAE, but the MS-like illness started earlier and was more severe in mice

without CNTF, according to a report in the June issue of the journal Nature

Medicine. The mice without CNTF experienced much more drastic destruction of

oligodendrocytes.

The researchers suspect that CNTF helps prevent myelin from being destroyed

by acting on a substance called tumor necrosis factor (TNF). When mice

lacking CNTF were treated with an antiserum that blocks TNF, the severity of

the disease was reduced.

CNTF may be just the tip of the iceberg, according to Gold. He told Reuters

Health that a number of other chemicals like CNTF may also have an effect on

the severity of MS. Eventually, it may be possible to combine some of these

chemicals, known as cytokines, with current MS therapy, Gold pointed out.

In another article in the same issue, Dr. Trevor J. Kilpatrick of the

University of Melbourne in Australia and associates report that a molecule

related to CNTF reduces demyelination in mice with EAE.

" We have found that administration of the molecule leukemia inhibitory

factor reduces the severity of demyelinating disease in a mouse model of

multiple sclerosis, " Kilpatrick told Reuters Health.

The significance of the finding, he said, is that leukemia inhibitory

factor, or LIF, works by preventing cell death, particularly of

oligodendrocytes, which are " specifically targeted in MS. " He noted that all

current MS therapies work by combating inflammation rather than by

preventing cell death.

Kilpatrick and his colleagues also found that the activation of LIF is a

normal part of the nervous system's response that limits the severity of an

injury. This discovery fits in well with the work by Gold's team that showed

that mice lacking CNTF, which Kilpatrick said is a " sister molecule " of LIF,

increases the severity of an MS-like illness in mice.

" CNTF and LIF and the receptors that they activate may be key determinants

of the severity of MS, " Kilpatrick said.

Currently, there is no appropriate therapy to treat the nerve cell death in

MS patients, according to the Australian scientist.

" LIF might, in principle, ultimately be attractive therapy in combination

with standard anti-inflammatory treatments, " he said.

SOURCE: Nature Medicine 2002;8:613-624.

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