News Neuronal Repair in MS May Be Triggered by an Inflammatory Molecule Neuronal Repair in MS May Be Triggered by an Inflammatory Molecule by Patricia Silva, PhD | January 15, 2016 Share this article: Share article via email Copy article link A new study fromĀ The Weizmann Institute of Science,Ā Israel, found that the inflammatory molecule CXCL12 promotes neuronal repair during spontaneous remission in mice with experimental autoimmune encephalomyelitis (EAE), an animalĀ model ofĀ human multiple sclerosis (MS). The chemokine CXCL12 was previously thoughtĀ to be a pro-inflammatory molecule only. But recent findings have shown that ā depending on interactions with other factors, as well asĀ the interactions’ timing and context ā CXCL12 could also beĀ anti-inflammatory and immunomodulating, and promote re-myelination. The research team induced EAEĀ in the mice and tracked the expression of CXCL12 in their brains, both during disease development and in the period of spontaneous remission. Researchers observed that levels of the molecule increased steadily while the disease advanced, andĀ did not subside when the mice spontaneously recovered. Instead, the team found that the levels of the immune factor increased even further, even thoughĀ inflammation was no longer present in the brain. The levels of CXCL12 in mice recoveringĀ from EAEĀ were found to be significantly higher than in mice that had not experienced inflammation. The spontaneousĀ remissionĀ process was also accompanied by increased numbers of two cell typesĀ destined to turn into either new neurons orĀ oligodendrocyte cells. Oligodendrocytes are the main myelin producing cells inĀ the brain. A closer investigation of these cells showed that they were a source of CXCL12 and its receptor CXCR4. The results highlightedĀ the complexity of the immune response, showing that increased levels of immune molecules do not always contribute to pathology, but might be elevated to protect tissue, or ā as in this case ā triggering re-myelination and neuronal repair following inflammation. The findingsĀ offer an important insight into healing processes in the brain, which might be explored in further studies aiming to develop new MS treatments. The study,Ā “Post-CNS-inflammation expression of CXCL12 promotes the endogenous myelin/neuronal repair capacity following spontaneous recovery from multiple sclerosis-like disease,”Ā was led by Rina Zilkha-Falb from Sheba Medical Center and colleagues fromĀ The Weizmann Institute of Science, both in Israel, and theĀ Ludwig-Maximilians-University, Munich, Germany. It was published online in the Journal of Neuroinflammation. Print This Page About the Author Patricia Silva, PhD PatrĆcia holds a PhD in medical microbiology and infectious diseases from the Leiden University Medical Center, Netherlands, and completed a postdoctoral research fellowship at the Instituto de Medicina Molecular, Lisbon, Portugal. Her work in academia was mainly focused on molecular biology and the genetic traits of infectious agents such as viruses and parasites. PatrĆcia earned several travel awards to present her work at international scientific meetings. She is a published author of several peer-reviewed science articles.
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