Rheumatoid Arthritis – Central Nervous System works to monitor Inflammation

Rheumatoid Arthritis – Central Nervous System works to monitor Inflammation

Researchers from the University of California, San Diego (UCSD) School of Medicine demonstrated how rheumatoid arthritis inflammation of the joints are sensed and adjusted by the central nervous system (CNS). The CNS has a potential to directly control immune system responses. The study will be first published in the September edition of the journal Public Library of Science (PLoS) Medicine.

“The central nervous system is not just a passive responder to the outside world, but is fully able to control many previously unanticipated physiologic responses, including immunity and inflammation," said Gary S. Firestein, M.D., Professor of Medicine, Chief of the Division of Rheumatology, Allergy and Immunology, and Director of UCSD's Clinical Investigation Institute, who led the study.

"This is an entirely new approach," Firestein said. “Instead of targeting enzymes at the actual site of disease, our hypothesis is that the central nervous system is a controlling influence for the body and can regulate peripheral inflammation and immune responses."

There has been a large amount of research in ways to block the signaling enzyme called p38 MAP kinase in the body which is released in a reaction to stress that regulate inflammation in patients that suffer with arthritis. In rheumatoid arthritis p38 is known to control the production of a cytokine called TNFĄ. Researchers have focused on treating the inflammation at the location of the disease instead of in the CNS.

Both researchers, Linda Sorkin, Ph.D., Department of Anesthesiology and David L. Boyle, Department of Medicine believe that controlling rheumatoid arthritis by way of the CNS may be a more important treatment than originally thought.

In this study, the researchers were able to block a key signaling enzyme in the CNS of rats. By blocking this enzyme the rats had decreased joint inflammation and destruction.

“We observed that the p38 signal is turned on, or activated, in the central nervous system during peripheral inflammation," Firestein said. "If we blocked this enzyme exclusively in a highly restricted site but not throughout in the body, inflammation in the joints was significantly suppressed."

The rats that had the p38 inhibitors administered in the spinal fluid had less signs of arthritis and they also experienced less damage to the joints.

The researchers also tested TNFĄ to see how the rats would respond when delivered into the spinal fluid. They used a TNF-inhibitor that is approved for the treatment of rheumatoid arthritis which is usually given throughout the body. They introduced the TNF-inhibitor in the CNS used less amounts and was able to activate the p38. They were able to block the pathway in the spinal cord.

The researchers conclude that new anti-inflammatory drugs could be better directed at the central nervous system to treat rheumatoid arthritis. They also point out the complexity of how the CNS works with the body.



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