Pain alerts the body to danger, but UC San Francisco researchers report that it may play another crucial role - helping to prevent the body from slipping into the chronic inflammation associated with such diseases as arthritis, colitis and asthma.

The finding, published in the September issue of Nature Medicine, provides the first evidence -- after years of inquiry -- of an active process controlling inflammation, and may open a new window to understanding the mechanisms at the heart of chronic inflammatory diseases.

People experience pain when signals from specialized nerve fibers are activated. These pain nerve fibers are triggered when tissue is damaged. They are re-activated by inflammation, the body's normally beneficial response to trauma and infection.

Inflammation increases blood flow to the site of injury and sends in a flood of rescue factors - such as substances that clot wounds and white blood cells that chew up invading disease-causing pathogens -to the site. But research has shown that unrestrained inflammation can cause chronic, debilitating diseases.

Traditionally, researchers have thought that the factors involved in the inflammatory response ultimately dissipated on their own. But the UCSF study suggests that activated pain nerve fibers, themselves, dampen the inflammatory response's first line of attack -- a cell known as the neutrophil, which sweeps into an injured site, releasing chemicals that work to heal wounds.

"Our work suggests that pain acts as a negative feedback control of inflammation," said the lead author of the study, Holly Strausbaugh, PhD, a postdoctoral fellow in the NIH Pain Center at UCSF. "Once enough inflammation builds up that pain nerve fibers are activated, the inflammatory response begins to diminish. Failure of this mechanism could contribute to the development of chronic inflammatory disease."

Notably, said Strausbaugh, pain fibers are not activated until the inflammatory response is we
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Contact: Jennifer O'Brien
jobrien@pubaff.ucsf.edu
415-476-2557
University of California - San Francisco
30-Aug-1999