Peripheral neuropathy is a common neurological complication of diabetes, and about half of the patients develop neuropathic pain. Here, we propose that targeting the peripheral source of inflammatory mediators of pain in the skin may promote a homeostatic metabolic local milieu that disrupts the inflammatory cascade and relieve pain. 
We use skin fibroblasts collected at the site of pain to offer a unique cell model to study peripheral pain sensitization in patients with diabetes and painful neuropathy.
We have performed a preliminary study using the Luminex Multiplex Technology to investigate the inflammatory profile of the skin fibroblasts, and we find that skin fibroblasts derived from patients with diabetes and painful neuropathy show a substantial production and excretion of IL-6, even in the absence of stimulatory signals.