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Immune-response research may yield new pain treatment for herniated discs
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An immune cell known to cause chronic inflammation in autoimmune disorders has been identified as a possible culprit in low back pain associated with herniated discs, according to investigators at Duke University Medical Center.
The finding implicates the cytokine molecule interleukin-17, and supports the burgeoning theory that an immune response plays a significant role in disc disease, William J. Richardson, MD, an orthopedic surgeon at Duke, stated in a university press release. It may also open the door for new therapeutic approaches that target a specific immune response in hopes of halting disc destruction, and possibly reversing the disease process.
“By identifying the specific subpopulation of lymphocytes, it may soon be possible to arrest the body’s inflammatory response to disc cells,” stated Richardson, senior author of the research published online in the July issue of Arthritis and Rheumatism. Doing so could reduce the painful inflammation associated with degenerative disc disease, and halt the evolution of arthritis. It may also reduce the need for back surgery, according to the press release.
Pathways to block
“Mechanical forces may initiate the degenerative process, but biochemical inflammatory changes certainly play a role in disc pathology,” Mohammed Shamji, MD, PhD, a co-author of the study, stated in the release. Decreasing the inflammation may arrest or reverse the patient’s disease process and perhaps reduce the need for surgery. “Now we are learning which pathways we have to block.”
He continued, “The center of the disc is immune-privileged since it has never been exposed to the immune system. When a disc is injured or degenerates, the body reacts against the invading inner material as it would against any virus or foreign body, and launches a response targeted at destruction. The nerve root, which is present near the protruding disc material, becomes painfully inflamed, swollen and damaged during that cascade of events.”
Recently, several anti-immune therapies, including steroids, have been injected into the space between the disc and the nerve, but with limited success, doctors say, because they don’t target a specific immune response, and because low doses are used to minimize potentially serious side effects that include a higher predisposition to infection, activation of tuberculosis and a six-fold increase in lymphoma incidence.
Several steps away
The identification of interleukin -17 in the cascade of events is significant, Shamji said. “It’s a product of a specific subgroup of immune cells that are involved in auto immune phenomena like rheumatoid arthritis and asthma, but not in the body’s response against infection or tumor. If you target this specific lymphocyte, you may avoid compromising the body’s ability to protect itself against infection or tumor.”
The researchers noted they are still several steps away from human studies of interleukin -17 blockers currently in development.
- Reference:
Shamji MF, Setton LA, Wingrove J, et al. Proinflammatory cytokine expression profile in degenerated and herniated human intervertebral disc tissues. Arthritis Rheum. 2010;62(7):1974-1983.
