The Immunology of the CNS: Tracing Newfound Pathways to Pain

When you hear "T cell" or "interferon," most likely you think of inflammation and joints. But they and other immune-like factors are also present in the nervous system, and appear to play an important role in the pathogenesis of chronic pain syndromes.

In this brief recorded interview, immunologist Peter Grace PhD describes revelations from this recent line of research and their implications for understanding of centralized pain.

Lead author of a recent review on neuroimmunology in Nature Reviews Immunology, Dr. Grace earned his PhD at the University of Adelaide and is now a postdoctoral fellow in the Center for Neuroscience at the University of Colorado in Boulder.

Questions:

Your article ... is entitled "Pathological Pain and the Neuroimmune Interface." What is the neuroimmune interface?

What are these immune cells doing in the CNS?

So what does all of this tell us about the transition from acute to chronic pain in people who have chronic pain syndromes?

It sounds like this work is moving toward defining a mechanism that might explain some of the hypervigilance that doctors see in cases like fibromyalgia.

What are the challenges in translating this line of research into clinical benefit for patients in chronic pain?

Is this one of those concepts that's controversial or would you say that among scientists this is a well-accepted line of research?

Key quotes:

•  "There's no known antibody response or antigen presentation after nerve injury..."

•  "Mediators that are released by immune-like cells can actually mimic neurotransmitters or conversely they can inhibit or even enhance neurotransmitter action and by doing this can actually contribute to central sensitization which underlies many if not all chronic pain conditions."

•  "The question is why do [these cells] go on to get so hot and bothered and start spewing out cytokines, which actually cause more damage."

•  "We're only beginning to gain an appreciation for the fact that neurons aren't just passive recipients of immune signaling, that they are capable of modifying immune function."
 

References:

Grace PM, Hutchinson MR, Maier SF, and Watkins LR. Pathological pain and the neuroimmune interface.Nat Rev Immunol (2014) Epub ahead of print 28 Feb 2014. doi: 10.1038/nri3621 

Loram LC, Grace PM, Strand KA, et al.Prior exposure to repeated morphine potentiates mechanical allodynia induced by peripheral inflammation and neuropathy.Brain Behav Immun (2012) 26:1256–1264 

Loram LC, Taylor FR, Strand KA et al.Prior exposure to glucocorticoids potentiates lipopolysaccharide induced mechanical allodynia and spinal neuroinflammation.Brain Behav Immun (2011) 25:1408–1415

Hains LE, Loram LC, Taylor FR,  et al.Prior laparotomy or corticosterone potentiates lipopolysaccharide-induced fever and sickness behaviors. (2011) J Neuroimmunol 239:53–60