Fast facts about pain
For years, scientists have thought of pain as a consequence of inflammation. They defined pain as something that evolved out of necessity so that the body can have a means of warning the brain about a harmful stimulus. Pain also became the body's main SOS signal, which alerts the brain whenever a body part or organ is injured or unable to function properly.
Pain is broadly categorized into either nociceptive pain, neuropathic pain or "other" types of pain. Nociceptive pain refers to the kind of pain that arises from tissue injury and is reported to the brain by the nervous system. Neuropathic pain, on the other hand, is triggered when the nervous system itself sustains damage due to mechanical insults. Unlike nociceptive pain, neuropathic pain is often chronic as nerves don't heal very well.
Any kind of pain that does not fall under either category is classified as "other" types of pain. These are common kinds caused by issues known as functional pain disorders. One example of these is fibromyalgia (musculoskeletal pain), a nervous system dysfunction that causes widespread body pain and whose underlying mechanism is poorly understood. Fibromyalgia is not considered neuropathic because it develops in the absence of nerve injury.
But according to recent studies, pain has a broader function than just serving as a signal for tissue or nerve damage. Scientists are now learning that pain is also important for host defense and immunity against microbial pathogens. (Related: Pain got you down? Researchers find certain regions in the brain are involved in both pain and depressive mood.)
Pain-sensing nerve cells activate a new type of immunity
For their study, UPIT researchers developed an animal model in which pain-sensing neurons in the skin can easily be activated using blue light. In the absence of pathogens and through simple light stimulation, the researchers found that the activation of these neurons triggers the release of a protein called CGRP. CGRP has the ability to recruit immune cells wherever it is produced, suggesting that pain-sensing neurons in the skin can detect pathogens and activate an immune response that's different from the ones known to scientists.
In the presence of Candida albicans and Staphylococcus aureus, the researchers reported that the pain-sensing neurons initiated an immune response to fight the infection. The neurons also sent signals to the spinal cord, which then traveled back to the skin and activated immune defenses around the site of infection. This event, which the researchers dubbed "anticipatory immunity," was instrumental to the containment of the infection.
"This demonstrates that the immune and nervous systems work synergistically for host defense," said Daniel Kaplan, the senior author of the study. "These findings also could have important implications for developing more specific therapies for autoimmune skin diseases like psoriasis."
Lead author Jonathan Cohen also said that the nervous system's involvement in this particular scenario is advantageous, as the network of neurons found in the human body can communicate information in a matter of milliseconds. In comparison, immune cells need hours or days to do the same.
"Understanding this really new type of immunity raises the intriguing question of whether we could develop a drug to selectively suppress excessive autoimmune inflammation in specific tissues, avoiding the negative side effects that come with using a broad immunosuppressant that affects the entire body," Kaplan added.
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