NIPPS

Acute postsurgical pain results from iatrogenic injuries to skin, muscle, fascia, and small nerve fibres innervating the injured tissues. It is observed in all patients undergoing surgical procedures and therefore represents a clinically relevant form of pain which requires immediate attention by the treating staff at surgery departments. Recent meta-analysis studies suggest that particularly after thoracotomy chronic pain rates are approximately 50 % up and have been stable from the 1990s to the present. Therefore, chronic pain after surgical interventions, in particular thoracotomy, continues to be a significant clinical problem despite advancing perioperative care. Although dysregulation of pro- and anti-inflammatory cytokines and inflammatory as well as neuropathic components have been associated with neuropathic and inflammatory pain, the mechanisms that are key for the transition from adaptive acute pain to maladaptive chronic pain are incompletely understood. It is therefore an urgent unmet medical need to address the mechanisms of postsurgical acute pain and risk factors for pain chronification. The NIPPS project will tackle these challenges and explore the role of neuroimmune interactions in pain sensing neurons, the nociceptors, in the generation of acute incisional pain and pathological pain in preclinical models. NIPPS will assess the involvement of novel neuroimmune regulators the microRNAs in neuroimmune interactions towards improved resolution of maladaptive pain

Acute postsurgical pain results from iatrogenic injuries to skin, muscle, fascia, and small nerve fibres innervating the injured tissues. It is observed in all patients undergoing surgical procedures and therefore represents a clinically relevant form of pain which requires immediate attention by the treating staff at surgery departments. Recent meta-analysis studies suggest that particularly chronic pain with a major neuropathic component develops in approximately 50 % of patients. Therefore, chronic pain after surgical interventions is a significant clinical problem despite advancing perioperative care. Although dysregulation of pro- and anti-inflammatory cytokines and inflammatory as well as neuropathic components have been associated with neuropathic and inflammatory pain, the mechanisms that are key for the transition from adaptive acute pain to maladaptive chronic pain are incompletely understood. It is therefore an urgent unmet medical need to address the mechanisms of postsurgical acute pain and risk factors for pain chronification. The NIPPS project has tackled these challenges and explored the role of neuroimmune interactions in pain sensing neurons, the nociceptors, in the generation of acute incisional pain and pathological pain in preclinical models. NIPPS finds the involvement of interleukin-6 signal transducer as an important regulator of neuroimmune crosstalk and reveals microRNA patterns associated with maladaptive pain in preclinical models.