Abstract: Abdominal pain is a common symptom associated with irritable bowel syndrome and inflammatory bowel diseases (IBDs), affecting about 20% of the global population (Grundy et al., 2019). Current pain therapies are poorly effective on visceral pain of intestinal origin and present several side effects, hence the need to identify novel molecular and cellular targets for drug development. The pathophysiology of visceral-abdominal pain, which often originates from the colorectal region, involves several actors, including the gut microbiome, intestinal epithelium, immune system, and nervous system at different levels through the gut-brain axis (Lucarini et al., 2020, 2022; Najjar et al., 2020). Nociceptive stimuli from the bowel to the central nervous system are mainly encoded by spinal afferents, whose cell bodies reside within the thoracolumbar and lumbosacral dorsal root ganglia (DRGs; Grundy et al., 2019). Visceral pain results from an altered neuronal transduction and transmission of stimuli generated within the gut. Current evidence attests that visceral hypersensitivity is a complex phenomenon, consisting of multiple mechanisms, with immune cells playing a role in hypersensitizing colon afferents through the release of different mediators (Grundy et al., 2019). However, pain is also reported without any inflammatory status, suggesting factors other than the inflammatory/immune signaling in driving pain transmission/persistence.