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Sep 19, 2013
 |  BC Innovations  |  Targets & Mechanisms

Bacteria's painful truth

In a surprise finding likely to alter how neurologists, immunologists and microbiologists view infection-associated pain, a group at Boston Children's Hospital has shown that bacteria can directly trigger action potentials in pain fibers, leading to the release of neuropeptides that suppress the inflammatory response.1 The findings point to a role for sensory neurons as immune modulators and could provide new bacterial targets for pain.

Until now, the immune system has been considered the primary instigator of pain from bacterial infections. Activation of immune cells triggers the release of inflammatory mediators such as cytokines, growth factors and prostaglandins, which are thought to cause pain by activating receptors on nerve terminals.

More recently, the recognition of bacterial patterns by toll-like receptors (TLRs) on sensory neurons has been pegged as an additional contributing mechanism, although the full picture remains unclear.2

Clifford Woolf and colleagues set out to shed some light on the mechanism by identifying specific inflammatory mediators responsible for acute bacterial pain. Unexpectedly, the team discovered that the pain and inflammatory responses were not coordinated and that the traditional model might not be accurate.

Woolf is director of the F.M. Kirby Neurobiology Center at Boston Children's Hospital and a professor of neurology and neurobiology at Harvard Medical School.

"The first major clue something interesting was going on was that the pain occurred out of sync with the immune response," Woolf told SciBX.

To identify pain-promoting cytokines active in the acute stage of bacterial infection, the group injected mice with a community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) strain linked to wound infections. The group then tracked the timing of pain response, mobilization of inflammatory markers and bacterial load.

The pain response peaked at six hours postinfection,...

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