Aspirin Suppresses MS Symptoms by Preventing Loss of Regulatory T-cells, Mouse Study Shows

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Aspirin, administered orally at low doses, was sufficient to suppress multiple sclerosis (MS) symptoms in a mouse model of relapsing-remitting MS (RRMS) and chronic MS, a study reports.

The clinical benefits of aspirin were linked to an increase in the number of regulatory T-cells, those responsible for shutting down overreactive immune responses (a hallmark of MS), via the increase of interleukin-11 (IL-11).

The study, “Aspirin ameliorates experimental autoimmune encephalomyelitis through interleukin-11–mediated protection of regulatory T cells,” was published in the journal Science Signaling.

A misguided and overactive immune response against myelin, the fat-rich substance that wraps around nerve fibers (axons), is the underlying mechanism of MS. This attack is mainly mediated by immune system cells called T-cells.

The immune system is tightly regulated, and since every immune response needs to come to an end, the body relies on a special group of cells called regulatory T-cells, or Tregs, which act as the “good police” and shut down the immune response triggered by overreacting T-cells.

However, in MS, there is a substantial decrease in the activity and number of Tregs.

Aspirin, whose active agent is acetylsalicylic acid, is probably the most used anti-inflammatory medicine, prompting a group of researchers to evaluate its immune modulatory effects in a well-established mouse model of MS called the experimental autoimmune encephalomyelitis (EAE) model.

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The team found that a low dose of oral aspirin suppressed the clinical symptoms of EAE in mouse models of both RRMS and chronic disease, compared with control (non-treated) EAE mice.

Aspirin had a marked effect in reducing the infiltration of inflammatory cells into the spinal cord, and prevented the loss of myelin.

To understand how aspirin protects from EAE disease, researchers evaluated how it affected the number and activity of Tregs, paying close attention to a subgroup of Tregs that have high levels of a transcription factor called Foxp3, previously shown to protect against EAE.

Results showed that aspirin prevented the loss of Tregs, and that this was the mechanism by which aspirin eases MS symptoms — depleting Tregs through a different approach erased the protective effects of aspirin on EAE mice.

Researchers then evaluated how aspirin affects a group of pro-inflammatory cells called Th17 and Th1 lymphocytes. Th17 cells play a key role in the destruction of the nerve cells’ protective myelin layer. The results showed that aspirin suppressed the development of both Th17 and Th1 cells, reducing inflammation and myelin damage.

Further experiments showed that the aspirin-induced increase in Treg numbers was mediated by the medicine’s effects in promoting the production of a signaling molecule called IL-11. In fact, IL-11 alone was sufficient to maintain the number of Foxp3-positive Tregs and protect mice from EAE.

“The effects of aspirin required the cytokine IL-11, which was itself sufficient to promote Treg stability and protect the mice from EAE development. These data suggest that low-dose aspirin regimens may benefit patients with MS,” the researchers wrote.

They concluded that the results “highlight an undiscovered property of aspirin and suggest the possibility that low-dose aspirin may be repurposed for therapeutic intervention in MS and other demyelinating conditions as an adjunct [add-on] therapy.”

Patricia holds her Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She also served as a PhD student research assistant in the Laboratory of Doctor David A. Fidock, Department of Microbiology & Immunology, Columbia University, New York.
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Patricia holds her Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She also served as a PhD student research assistant in the Laboratory of Doctor David A. Fidock, Department of Microbiology & Immunology, Columbia University, New York.
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