Translate
Translate this website into the following languages:



Close Tab
Donations
UC San Diego Health
menu iconMenu
search iconSearch

Starving Inflammatory Immune Cells Slows Damage Caused by Multiple Sclerosis

 

September 01, 2011  |  

In a paper published today in the journal Scientific Reports, a pair of researchers at the University of California, San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences report that inhibiting the ability of immune cells to use fatty acids as fuel measurably slows disease progression in a mouse model of multiple sclerosis (MS).

MS is an autoimmune disease resulting from damage to the myelin sheath, a protective layer surrounding nerve cells. When the sheath is damaged, nerve impulses are slowed or halted, resulting in progressive physical and neurological disabilities. The cause of the damage is inflammation occurring when the body’s immune cells attack the central nervous system (CNS).

Myelinated nerve

Nerve cell with protective layers of myelin.


Marianne Manchester, PhD, professor of pharmacy and first author Leah P. Shriver, PhD, looked at how immune cells in the CNS oxidize fatty acids for energy when their preferred fuel source – glucose – is in short supply, which may occur in inflamed tissues. In a mouse model  mimicking chronic MS, Manchester and Shriver discovered that by inhibiting a single enzyme that helps immune cells effectively exploit fatty acids, the cells eventually starved and died,  preventing further inflammatory damage.

Currently, no approved drug or therapy for MS targets fatty acid metabolism. And the specificity of the target – inhibiting a single enzyme – suggests that adverse side effects associated with existing treatments, such as increased infection risk, is unlikely.

“We expect that because immune cells not in lesions in the CNS are able to use available glucose, they will function just fine during infection and that inhibition of this pathway would not produce general immune suppression,” Shriver said.

The enzyme-inhibitor used by Manchester and Shriver in their study is a drug already tested in humans with congestive heart failure, and was generally well-tolerated. The scientists are now using mass spectrometry to determine whether their results in the mouse model are translatable to humans.  “We are interested in determining how this pathway is utilized in human tissue samples from MS patients,” Manchester said.

Funding for this study came from the National Institutes of Health and the National Institute of Neurological Disorders and Stroke.

# # #

Media Contact: Scott LaFee, 619-543-6163, slafee@ucsd.edu


Related Specialties



Media Contact

Share This Article


Related News

3/23/2017
From virtual reality to crowdsourcing ideas, participants at UC Health Hack 2017 combined creativity and problem-solving to create projects addressing critical issues in health systems and global heal ...
3/23/2017
In a new paper, researchers at University of California San Diego School of Medicine, along with colleagues in Brazil and Spain, describe the phenotypic spectrum or set of observable characteristics o ...
3/21/2017
In a new study, researchers at the University of California San Diego School of Medicine, University of Cyprus and Stanford University map the complex biological cascade caused by MIA: the expression ...
3/21/2017
Standard antidepressant medications don’t work for everyone, and even when they do they are slow to kick in. In an effort to find better depression treatments, researchers at University of California ...



Follow Us

Our bimonthly newsletter delivers healthy lifestyle tips, patient stories and research discovery news. Subscribe: