Chronic pain is a major global health burden that results in hypersensitivity to sensory input allowing normally innocuous stimuli to become painful. Many chronic pain states are linked to neural circuit dysfunction, which can be traced back to the spinal level in the majority of cases. In this study we investigated the mechanism underlying analgesic effects of a high-amylose diet in rodent models of fibromyalgia and arthritis. We have found that diet-induced changes to the gut microbiota reduce hyperexcitability in spinal nociceptive circuits and acts to relieve inflammation induced sensitivity. This was driven by a reduction in the activation and infiltration of inflammatory cells in the spinal dorsal horn and a reduction in the expression of neurotrophic factors in the peripheral sensory neurons. Cytokine expression was changed in these regions leading to a reduction of pronociceptive cytokines and inflammation. Electrophysiological studies showed that the acetate diet restored the excitatory-inhibitory balance in neuronal activity in sensory circuits and reduced central sensitization. These findings show that modification of gut microbiota may provide a safe and effective therapeutic option for the treatment of chronic inflammatory pain conditions.