Inflammatory pain may help deter inflammatory diseases like arthritis

ll under way, which gives the inflammatory response time to mount a powerful attack first. "It's a neat little trick, because some inflammation is good. It just needs to be kept in check," she said. Strausbaugh conducts her research in the laboratory of senior author Jon Levine, MD, PhD, a professor of medicine and oral and maxillofacial surgery and director of the NIH Pain Center at UCSF.

"If we can understand what factors mediate the response we're seeing from the pain circuit -- down to the molecular mechanisms -- then we can eventually start looking in people who have chronic inflammatory diseases to try to see if the mechanism is disrupted there. If we find that it is, we can try to fix it," she said.

As neutrophils play a central role in inflammatory responses throughout the body, the researchers' observation will likely apply to inflammation across the board, said Strausbaugh, though, she added, painful stimuli will likely prove to be one of several factors modulating the inflammatory response.

The researchers conducted their study in anesthetized rats with inflamed knee joints, determining that a painful stimulus applied to the animals' hind paw completely blocked neutrophil accumulation in the animals' joints. Researchers in the Levine lab had previously shown that activated pain fibers in the rats' hind paw caused decreased swelling in the animals' inflamed knee joints. This decrease in swelling, far from the site where the nerve fibers were activated, had indicated that the nerves were exerting their effects through some factor that had access to or could migrate to a different part of the body.

And it was this observation that suggested the possible role of the roving neutrophils.

The current study demonstrated not only that neutrophils were the target of the activated pain nerve fibers, but that the pain fibers acted on these cells through the leukocyte adhesion molecule known as L-selectin. Neutrophils access inflammation by mo

Contact: Jennifer O'Brien
University of California - San Francisco

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