Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain. Thus, pain helps the organism avoid noxious stimuli.
The immune system plays an essential role in pain pathology. Upon encountering noxious stimuli, immune cells such as mast cells and macrophages present at the site of injury release inflammatory chemicals such as cytokines, chemokines, histamines, and prostaglandins. These chemicals attract other immune cells such as monocytes and T cells to the injury site. They also stimulate nociceptors, resulting in hyperalgesia—a more intense response to a previously painful stimulus, or allodynia—a painful response to a normally innocuous stimulus such as light touch. Such pain sensitization helps protect the injured site during healing.
In some cases, pain outlives its role as an acute warning system if sensitization fails to resolve over time. Chronic pain—persistent or recurrent pain lasting longer than three months—often accompanies inflammatory conditions such as rheumatoid arthritis. Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen reduce pain by inhibiting the synthesis of the inflammatory molecules prostaglandins. However, NSAIDs and opioids currently used to combat pain suffer from severe side effects and the potential for addiction. Therefore, understanding the mechanisms underlying pain pathology can help develop more effective drugs to suppress pain perception with less severe negative side effects.
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