Over 50 million Americans suffer from autoimmune diseases, and while we are learning more about how to manage symptoms, we still don’t fully comprehend the basics.

The new research has found an important way that Adenosine triphosphate (ATP), a neurotransmitter that increases inflammation and is released when sensory neurons and interneurons talk to each other.

This is significant for the spread of inflammation between joints.

Rheumatoid arthritis is an autoimmune disease that causes chronic inflammation in the joints. Remote inflammation, in which inflammation extends from one joint to another, is one of the disease’s hallmarks. Inflammation spread is thought to be aided by neuronal circuits or cells migrating from the joints, although the precise process by which this occurs has yet to be discovered.

Professor Masaaki Murakami of Hokkaido University led a team of researchers from Japan and the United States to discover that remote inflammation is propagated via neuron crosstalk, and that adenosine triphosphate (ATP) plays a critical role in this process. Their findings, which were published in the Journal of Experimental Medicine, could lead to new inflammatory disease medicines and treatments.

Inflammation is a part of the immune system’s normal response to infection or irritation. It is a process in which the immune system seeks to eliminate pathogens and damaged cells using immune cells, blood vessels, and molecular mediators, and then heal the harm. Excessive inflammation, on the other hand, is a condition in and of itself, as observed in diseases like hay fever, atherosclerosis, psoriasis, and rheumatoid arthritis, to name a few.

The authors of this study hypothesized that neural crosstalk could be responsible for remote inflammation based on previous observations of the gateway reflex—an immune response mechanism in which specific neural signals change the state of specific blood vessels to allow immune cells to enter tissue, resulting in local inflammation.

They put this theory to the test using mice models of rheumatoid arthritis. The mice were split into two groups: control and test. The sensory neuronal connections between the left and right ankle joints were disrupted in the test groups. Both pairs of mice were subsequently given arthritis in the left ankle, and the spread of arthritis to the right ankle was noted.

Their findings revealed that a sensory neuron link in the spinal cord transmits an inflammation signal from one joint to the other, causing inflammation in both joints. Inflammation in one joint caused a rise in ATP in both joints, which led to an increase in a signal molecule that caused inflammation. The spread of inflammation was stopped by blocking this route.

Because this research was done on mice, more research is needed to see if the findings extend to human rheumatoid arthritis and other chronic inflammatory disorders. If that’s the case, it could be a therapeutic target for a variety of disorders characterized by widespread inflammation.

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