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  • Title: Interleukin-1alpha regulates substance P expression and release in adult sensory neurons.
    Author: Skoff AM, Zhao C, Adler JE.
    Journal: Exp Neurol; 2009 Jun; 217(2):395-400. PubMed ID: 19341730.
    Abstract:
    Nerve injury frequently results in development of chronic, dysesthetic pain and allodynia (painful sensation in response to benign stimulation). Following nerve injury, spinal cord glia become activated and secrete a number of inflammatory cytokines, including interleukin-1 (IL-1), which exists as two genetically distinct proteins, IL-1alpha and IL-1beta. To investigate whether neuropeptide expression could be altered by exposure to these cytokines, dorsal root neurons from mature rats were grown in culture and substance P (SP) expression was analyzed. IL-1alpha and IL-1beta both increased neuronal content of SP. Interestingly, IL-1alpha was significantly more efficient than IL-1beta in inducing SP expression. Cultured neurons exposed to either cytokine secreted substantially more SP with capsaicin stimulation than did control cultures, supporting a physiologic role for these inflammatory cytokines after nerve injury. However, when IL-1beta was added in combination with IL-1alpha to cultured neurons, the amount of SP expressed was significantly lower than that induced by IL-1alpha alone. Evidence is presented that both cytokines alter SP expression via the IL-1 receptor, and that the signaling pathway involves nerve growth factor (NGF) expression and transcription. In summary, IL-1alpha was significantly more efficient than IL-1beta at up-regulating SP expression than IL-1beta. Taken together, these observations suggest an important role for IL-1alpha in the events following nerve injury.
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