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Acyloxyacyl hydrolase is a host determinant of gut microbiome-mediated pelvic pain

Title: Acyloxyacyl hydrolase is a host determinant of gut microbiome-mediated pelvic pain
Authors: Rahman-Enyart, Afrida; Yang, Wenbin; Yaggie, Ryan E.; White, Bryan A.; Welge, Michael; Auvil, Loretta; Berry, Matthew; Bushell, Colleen; Rosen, John M.; Rudick, Charles N.; Schaeffer, Anthony J.; Klumpp, David J.
Contributors: Pharmacology and Toxicology, School of Medicine
Source: PMC
Publisher Information: The American Physiological Society
Publication Year: 2021
Collection: Indiana University - Purdue University Indianapolis: IUPUI Scholar Works
Subject Terms: Acyloxyacyl hydrolase; Gut dysbiosis; Interstitial cystitis; Microbiome; Pelvic pain
Description: Dysbiosis of gut microbiota is associated with many pathologies, yet host factors modulating microbiota remain unclear. Interstitial cystitis/bladder pain syndrome (IC/BPS) is a debilitating condition of chronic pelvic pain often with comorbid urinary dysfunction and anxiety/depression, and recent studies find fecal dysbiosis in patients with IC/BPS. We identified the locus encoding acyloxyacyl hydrolase, Aoah, as a modulator of pelvic pain severity in a murine IC/BPS model. AOAH-deficient mice spontaneously develop rodent correlates of pelvic pain, increased responses to induced pelvic pain models, voiding dysfunction, and anxious/depressive behaviors. Here, we report that AOAH-deficient mice exhibit dysbiosis of gastrointestinal (GI) microbiota. AOAH-deficient mice exhibit an enlarged cecum, a phenotype long associated with germ-free rodents, and a "leaky gut" phenotype. AOAH-deficient ceca showed altered gene expression consistent with inflammation, Wnt signaling, and urologic disease. 16S sequencing of stool revealed altered microbiota in AOAH-deficient mice, and GC-MS identified altered metabolomes. Cohousing AOAH-deficient mice with wild-type mice resulted in converged microbiota and altered predicted metagenomes. Cohousing also abrogated the pelvic pain phenotype of AOAH-deficient mice, which was corroborated by oral gavage of AOAH-deficient mice with stool slurry of wild-type mice. Converged microbiota also alleviated comorbid anxiety-like behavior in AOAH-deficient mice. Oral gavage of AOAH-deficient mice with anaerobes cultured from IC/BPS stool resulted in exacerbation of pelvic allodynia. Together, these data indicate that AOAH is a host determinant of normal gut microbiota, and dysbiosis associated with AOAH deficiency contributes to pelvic pain. These findings suggest that the gut microbiome is a potential therapeutic target for IC/BPS.
Document Type: article in journal/newspaper
File Description: application/pdf
Language: English
Relation: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology; https://hdl.handle.net/1805/35297
Availability: https://hdl.handle.net/1805/35297
Rights: Publisher Policy
Accession Number: edsbas.B6E89EEF
Database: BASE