---
title: "Microglial TLR4 Drives Post‑UTI Chronic Pelvic Pain via Persistent Microglial Activation"
id: "biorxiv-5-microglial-tlr4-mediates-post-uti-chronic-pelvic-pain"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-5-microglial-tlr4-mediates-post-uti-chronic-pelvic-pain"
content_type: "clinical_feed_article"
specialty: "Neurology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.08.04.742321v1?rss=1"
published_at: "2026-08-10T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Microglial TLR4 Drives Post‑UTI Chronic Pelvic Pain via Persistent Microglial Activation
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-5-microglial-tlr4-mediates-post-uti-chronic-pelvic-pain
- **Specialty:** [Neurology](https://medichelpline.com/clinical-feed/neurology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.08.04.742321v1?rss=1)
- **Published At:** 2026-08-10T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Urinary tract infection (UTI) is a major risk factor for interstitial cystitis/bladder pain syndrome and can lead to persistent pelvic pain in a mouse model described as post‑UTI chronic pelvic pain (PUPP). - The study used an Escherichia coli infection to induce long‑lasting **pelvic allodynia** in mice, modeling chronic pelvic pain after UTI. - Pharmacologic depletion of microglia with PLX5622 or inhibition with minocycline significantly attenuated persistent pelvic pain, implicating **microglia** in pain maintenance. - Microglial depletion did not improve urinary dysfunction measures or anxiety‑ and depression‑like behaviors, indicating a dissociation between pain and these other outcomes in the model. - Prefrontal cortex microglia from PUPP mice showed reduced branching complexity and a less ramified morphology, consistent with an **activated microglial** phenotype. - Transcriptomic profiling of brain CD11b+ cells revealed a reactive microglial transcriptional signature enriched for chemokines, NFκB‑related genes, and immediate early response genes, and pathways linked to immune regulation and leukocyte recruitment. - Both constitutive (general) and microglia‑specific deletion of **TLR4** decreased pelvic allodynia and reduced microglial morphological activation features, implicating **microglial TLR4** as a mediator of post‑UTI chronic pelvic pain. - In vitro pharmacological inhibition of TLR4 suppressed LPS‑induced NFκB activation, cytokine secretion, and CD68 expression, consistent with TLR4 mediating microglial inflammatory responses relevant to pain. - The findings identify **microglial TLR4** as a critical mediator of persistent pelvic pain after UTI and suggest microglial activation and TLR4 signaling as potential mechanistic targets; the article is a preprint and has not been peer reviewed.
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Habib Jmii Northwestern University * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Habib%2BJmii%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Jmii%20H&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AHabib%2BJmii%2B) * [ORCID record for Habib Jmii](http://orcid.org/0000-0001-5254-5270 "Open in new tab") Shivesh Ghura Northwestern University * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Shivesh%2BGhura%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Ghura%20S&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AShivesh%2BGhura%2B) Anthony Schaeffer Northwestern University * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Anthony%2BSchaeffer%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Schaeffer%20A&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAnthony%2BSchaeffer%2B) David Klumpp Northwestern University * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=David%2BKlumpp%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Klumpp%20D&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ADavid%2BKlumpp%2B) * For correspondence: d-klumpp@northwestern.edu * [Abstract](https://www.biorxiv.org/content/10.64898/2026.08.04.742321v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5694622/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.08.04.742321v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5694622/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.08.04.742321v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5694622/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.08.04.742321v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5694622/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.08.04.742321v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5694622/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Urinary tract infections (UTIs) are a major risk factor for interstitial cystitis/bladder pain syndrome (IC/BPS), yet the mechanisms driving chronic pelvic pain and associated symptoms remain poorly understood. Here, we investigated the role of microglia and Toll-like receptor 4 (TLR4) in a mouse model of post-UTI chronic pelvic pain (PUPP). Infection with E. coli induced persistent pelvic allodynia that was significantly attenuated by microglial depletion (PLX5622) or inhibition (minocycline), indicating a key role for microglia in pain maintenance. In contrast, microglial depletion did not improve urinary dysfunction or anxiety- and depression-like behaviors. Prefrontal cortex microglia of PUPP mice exhibited reduced microglial branching complexity and a less ramified phenotype, indicative of an activated microglial state. Transcriptomic profiling of brain CD11b+ cells revealed a reactive microglial signature enriched for chemokines, NFΚB-related genes, and immediate early response genes, alongside pathways involved in immune regulation and leukocyte recruitment. Both general and microglia-specific TLR4 deletion reduced pelvic allodynia and reduced microglial morphological features of activation. Consistent with this, pharmacological TLR4 inhibition in vitro suppressed LPS-induced NFΚB activation, cytokine secretion, and CD68 expression. Together, these findings identify microglial TLR4 as a critical mediator of post-UTI chronic pelvic pain. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared National Institutes of Health, https://ror.org/01cwqze88, NIDDK 1R01DK134817 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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[ Download PDF](https://www.biorxiv.org/content/10.64898/2026.08.04.742321v1.full.pdf) Print/Save Options [Download PDF](https://www.biorxiv.org/content/biorxiv/early/2026/08/10/2026.08.04.742321.full.pdf)Full Text & In-line FiguresXML [More Info](https://www.biorxiv.org/about/FAQ#PrintOptions "More Information on Print/Save Options") [Supplementary Material ](https://www.biorxiv.org/content/10.64898/2026.08.04.742321v1.supplementary-material) [ Email](https://www.biorxiv.org/ "Email this Article") [ Share](https://www.biorxiv.org/) Microglial TLR4 Mediates Post-UTI Chronic Pelvic Pain Habib Jmii, Shivesh Ghura, Anthony Schaeffer, David Klumpp bioRxiv 2026.08.04.742321; doi: https://doi.org/10.64898/2026.08.04.742321 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. 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