Glial and immune cells; long regarded as passive bystanders in the nervous system, are now recognized as active architects of pain. In visceral and pelvic pain conditions, where persistent discomfort and hypersensitivity frequently outlast any detectable tissue injury, non-neuronal cells such as microglia, astrocytes, satellite glial cells, enteric glia, mast cells, and macrophages are increasingly implicated in the onset and maintenance of chronic sensitization. Disorders including irritable bowel syndrome, endometriosis-associated pain, interstitial cystitis, and chronic pelvic pain syndrome (CPPS) are all characterized by varying degrees of neuroimmune dysregulation, yet the precise cellular and molecular mechanisms remain poorly defined. Closing this gap is critical, not only for understanding why these conditions are so difficult to treat, but also for identifying new therapeutic targets in a patient population that remains significantly underserved.
This Research Topic seeks to bring together cutting-edge work that illuminates the roles of glial and immune cells across the full spectrum of visceral and pelvic pain. The collection will address key unresolved questions: How do spinal microglia and astrocytes amplify or sustain visceral nociceptive signals? What drives peripheral immune cell recruitment to visceral tissues, and how does this fuel afferent sensitization? How do enteric glial cells regulate gut–brain pain pathways, and how is this shaped by the microbiome? We are particularly interested in studies that shed light on sex differences in neuroimmune responses -an important dimension given that many visceral and pelvic pain disorders disproportionately affect women. The collection also welcomes translational and clinical research identifying glial or immune biomarkers of disease progression, as well as work evaluating therapies that target neuroinflammatory pathways. Together, these contributions aim to reframe visceral and pelvic pain as a neuroimmune disorder and drive a new generation of mechanism-based treatments.
We invite Original Research, Review articles, Mini-Reviews, Systematic Reviews, Meta-analyses, Perspectives, and Opinion pieces addressing glial and immune cell involvement in visceral and pelvic pain.
Key thematic areas include: - Microglial and astrocyte roles in central sensitization to visceral stimuli - Satellite glial cells in dorsal root ganglia and pelvic pain signaling - Enteric glial contributions to gut pain and the gut–brain axis - Peripheral immune cell (mast cell, macrophage, T cell) involvement in visceral afferent sensitization - Neuroimmune crosstalk and neuroinflammation in CPPS and related syndromes - Microbiome–glial–immune interactions in chronic abdominal and pelvic pain - Sex-specific neuroimmune mechanisms in visceral pain disorders - Glial and immune biomarkers for diagnosis or patient stratification - Therapeutic targeting of neuroinflammatory pathways in pelvic pain
Submissions should offer mechanistic, translational, or clinical insights that advance understanding of visceral and pelvic pain through a neuroimmune lens, consistent with the Abdominal and Pelvic Pain section of Frontiers in Pain Research.
Article types and fees
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
Brief Research Report
Case Report
Clinical Trial
Data Report
Editorial
FAIR² Data
General Commentary
Hypothesis and Theory
Methods
Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.
Article types
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.