Are sensory neurons exquisitely sensitive to interleukin 1β?

Peripheral nerve injury frequently evokes chronic neuropathic pain. This is initiated by a transient inflammatory response that leads to persistent excitation of dorsal root ganglion (DRG) neurons by inflammatory cytokines such as interleukin 1 beta(IL-1 beta). In non-neuronal cells such as lymphocytes, interleukin 1 exerts actions at attomolar (aM; 10(-18) M) concentrations. We now report that DRG neurons in defined-medium, neuron-enriched culture display increased excitability following 5-6 d exposure of 1aM IL-1 beta. This response is mediated in part by type 1 interleukin receptors and involves decreased function of putative K(Ca)1.1 channels. This finding provides new insights into the neuroimmune interactions responsible for neuropathic pain.

Automated summary

Peripheral nerve injury often leads to chronic neuropathic pain, which is initiated by an inflammatory response that causes persistent excitation of neurons. This study reveals the impact of 1aM IL-1β on the excitability of neurons, potentially mediated through type 1 interleukin receptors.