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Urinary Bladder Distention Evoked Visceromotor Responses as a Model for Bladder Pain in Mice
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Gut Microbiome-Driven Microglial Activation Links Dysbiosis to Pain in Interstitial Cystitis/Bladder Pain Syndrome

Shivesh Ghura1, Habib Jmii1, James Griffith2

  • 1Northwestern University.

Research Square
|May 4, 2026
PubMed
Abstract

Insights

Gut bacteria in interstitial cystitis/bladder pain syndrome (IC/BPS) patients activate microglia, the brain's immune cells. This activation correlates with pain severity, suggesting a gut-brain axis link and potential microbiome-based therapies for IC/BPS.

Area of Science:

  • Neuroimmunology
  • Gastroenterology
  • Urology

Background:

  • Interstitial cystitis/bladder pain syndrome (IC/BPS) is linked to chronic pelvic pain, urinary frequency, anxiety, and depression.
  • Fecal dysbiosis and endotoxin exposure in IC/BPS patients may trigger central nervous system innate immune responses via microglial activation.
  • Microglia are key pain mediators, and their inactivation has shown analgesic effects in preclinical models.

Purpose of the Study:

  • To investigate if fecal microbiota from IC/BPS patients differentially activate microglia compared to controls.
  • To determine if microglial activation correlates with IC/BPS patient symptom severity.

Main Methods:

  • Utilized three in vitro culture models: BV2 cells, primary microglia, and mixed glial cultures (microglia and astrocytes).
  • Exposed microglial cultures to heat-killed, stool-derived microbiota from IC/BPS patients and controls.
  • Quantified pro-inflammatory cytokines (TNF-α, RANTES/CCL5, IL-6) using ELISA and correlated levels with patient-reported Genitourinary Pain Index (GUPI) scores.

Main Results:

  • Microglia showed significantly increased pro-inflammatory responses to IC/BPS patient microbiota across all culture models.
  • Mixed glial cultures, involving astrocyte-microglia interactions, demonstrated the most pronounced cytokine responses.
  • Elevated cytokine levels positively correlated with higher GUPI pain scores in IC/BPS patients.

Conclusions:

  • Findings support a role for gut dysbiosis in IC/BPS symptoms.
  • Microglial activation and glial-glial interactions represent a potential contributing mechanism to IC/BPS pain.
  • Understanding gut-brain axis interactions is crucial for developing novel microbiome-based therapies for IC/BPS.
Keywords:
Bladder Pain SyndromeGenitourinary Pain Index (GUPI)Gut microbiomeInterstitial CystitisMicrogliaNeuroinflammationPelvic Pain

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