U. scientists develop cell therapy for chronic disc pain

U. scientists develop cell therapy for chronic disc pain


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SALT LAKE CITY — Relief for chronic back and neck pain may be on the horizon, thanks to emerging science technology under development at the University of Utah.

Bioengineering researchers have discovered a technique to control chronic pain by regulating genes that reduce tissue- and cell-damaging inflammation.

“This has applications for many inflammatory-driven diseases,” said assistant professor Robby Bowles, who led the research. “It could be applied for arthritis or to therapeutic cells that are being delivered to inflammatory environments that need to be protected from inflammation.”

In laymen’s terms, the therapy has the potential to treat chronic pain by relieving swelling in affected areas and healing the tissue, he said.

For instance, chronic pain in slipped or herniated discs result from damaged tissue when swelling causes cells to create molecules that break down tissue, he explained. Inflammation is nature’s way of alerting the immune system to repair tissue or fight infection, but chronic inflammation can lead to tissue degeneration and pain, he said.

Bowles’ team uses the Clustered Regularly Interspaced Short Palindromic Repeat system — known as CRISPR — a new technology that modifies human genetics to halt cell death and keep cells from producing molecules that damage tissue and result in chronic pain, he said.

“This is something that could be injected into your (damaged) discs to stop the signaling that is driving disc degeneration and the painful signaling,” Bowles said. “It would keep you from getting worse and it would stop the pain.”

But Bowles said the therapy does not edit or replace genes, which is what CRISPR tools are typically used for. Instead, the therapy modulates the way genes turn on and off in order to protect cells from inflammation.

“So they won’t respond to inflammation. It disrupts this chronic inflammation pattern that leads to tissue degeneration and pain,” he said. “We’re not changing what is in your genetic code. We’re altering what is expressed. Normally, cells do this themselves, but we are taking engineering control over these cells to tell them what to turn on and turn off.”

He said now that researchers know they can do this, doctors would be able to modify the genes using direct injection into the affected area which delays tissue degeneration. In the case of back pain, a patient may get a discectomy to remove part of a herniated disc to relieve the pain, but tissue near the spinal cord may continue to break down, leading to future pain, he said. This method could stave off additional surgeries by stopping the tissue damage, he noted.

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“The hope is that this stops degeneration in its tracks, and the patient could avoid any future surgeries,” Bowles said. “But it’s patient to patient. Some might still need surgery, but it could delay it.”

So far, the team has developed a virus that can deliver the gene therapy and has filed for a patent on the system with the hope of moving to human trials after collecting initial data. One caveat Bowles noted was that there are currently no gene therapies approved for use by the U.S. Food and Drug Administration, so it may take some time to receive necessary acceptance.

“So long term there are technological and regulatory hurdles to (overcome),” he said. It could be about 10 years before this method is ready for use in patients.

Despite the regulatory issues, Bowles was optimistic about the long-range prospects for treating pain using this new therapy.

“The CRISPR systems give us control that would allow us to begin treating these diseases in ways we couldn’t treat them before,” Bowles said. “Over the next 10 to 15 years, we’re going to see a lot of these CRISPR technologies change these debilitating conditions.”

The team’s discovery was published in a new paper this month in a special issue of “Tissue Engineering.” The study was co-authored by University of Utah bioengineering doctoral student Niloofar Farhang and several other researchers in a collaborative project between the U., Duke University and Washington University in St. Louis.

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Jasen Lee


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