The findings, published Oct. 23 in the journal Science Immunology, also point to a potential way to block that pain.
"What we found is that the tissue itself changes consistency," Xu told Live Science in an email. "It becomes stiff and less elastic, a bit like a scar, and that stiffness alone keeps triggering the alarm even after the fire is out."
They zoomed in on a protein called Piezo1; in immune cells, it's known to play a role in inflammation, and in neurons, it contributes to pain signals. The team looked at whether this protein's activity changed in the context of colitis.
"They sit touching the nerve endings," Xu added.
They also measured pain levels in both sets of mice. "In mice with almost no visible gut inflammation, the pain was still there, which is why a colonoscopy can look normal while the patient hurts," Xu said.
That's because calcium ions rush into the cell via the channel, and that surge sends a protein called NF-kB from the cell's interior fluid into its nucleus — the control center where DNA is stored. There, NF-kB plugs into a gene, ordering the cell to manufacture nerve growth factor (NGF) that then exits the immune cell.
This newly described mechanism could help explain why ulcerative colitis patients can sometimes contend with pain even when their colonoscopies look normal. (Image credit: Kinga Krzeminska via Getty Images)
The researchers used chemicals as on-off switches for Piezo1 in immune cells, opening the channel with one and closing it with another. As they did this, they tracked calcium signals and NGF production, and both rose and fell in step with the switch. This result suggests that Piezo1 activity is both necessary for this response and, on its own, enough to trigger it in these cells, Xu said.
The study was "well controlled," said Hongzhen Hu, the scientific director for the Mark Lebwohl Center for Neuroinflammation and Sensation at the Icahn School of Medicine at Mount Sinai, who was not involved in the research. Future research should address the chemical messengers that coordinate inflammation, called cytokines, and determine whether the same chain reaction occurs in human cells, he said in an email.
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Other scientists have explored using anti-NGF treatments for other chronic pain conditions but not for ulcerative colitis, Xu noted. Fully blocking NGF might have downsides, he said, since NGF also helps to maintain nerves.
"For the pain field, that's a conceptual shift," Xu said.
This article is for informational purposes only and is not meant to offer medical advice.
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