ArticlePloS one2012
O-antigen modulates infection-induced pain states.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05306314 (A Study to Understand the Treatment Patterns in Patients With Chronic Bacterial Prostatitis), which is not on this map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Study to Understand the Treatment Patterns in Patients With Chronic Bacterial Prostatitis (Category II), Chronic Pelvic Pain (Category IIIA, IIIB)Treataprost Added to Standard Antibiotic Treatment in Real-life Clinical Practice
Who cites it
24 citing papers in PubMed, 48 citations in OpenAlex.
- The gut-brain axis and pain signalling mechanisms in the gastrointestinal tract.Nature reviews. Gastroenterology & hepatology · 2025Review
- Article
- Acyloxyacyl hydrolase is a host determinant of gut microbiome-mediated pelvic pain.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- The role of the vaginal microbiome in distinguishing female chronic pelvic pain caused by endometriosis/adenomyosis.Annals of translational medicine · 2021Article
- UPEC kidney infection triggers neuro-immune communication leading to modulation of local renal inflammation by splenic IFNγ.PLoS pathogens · 2021Article
- Microbiota-neuroimmune cross talk in stress-induced visceral hypersensitivity of the bowel.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Urologic chronic pelvic pain syndrome: insights from the MAPP Research Network.Nature reviews. Urology · 2019Review
- An Overview of the Pathology and Emerging Treatment Approaches for Interstitial Cystitis/Bladder Pain Syndrome.Cureus · 2018Review
- Neuroepithelial control of mucosal inflammation in acute cystitis.Scientific reports · 2018Article
- TRPV1 and the MCP-1/CCR2 Axis Modulate Post-UTI Chronic Pain.Scientific reports · 2018Article
- Acyloxyacyl hydrolase modulates pelvic pain severity.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Infection, Pain, and Itch.Neuroscience bulletin · 2018Review
- Staphylococcus aureus produces pain through pore-forming toxins and neuronal TRPV1 that is silenced by QX-314.Nature communications · 2018Article
- How Often Do Clinically Diagnosed Catheter-Associated Urinary Tract Infections in Nursing Homes Meet Standardized Criteria?Journal of the American Geriatrics Society · 2017Article
- Gut microbiome and chronic prostatitis/chronic pelvic pain syndrome.Annals of translational medicine · 2017Review
- The unexplored relationship between urinary tract infections and the autonomic nervous system.Autonomic neuroscience : basic & clinical · 2016Review
- Dectin-2 Recognizes Mannosylated O-antigens of Human Opportunistic Pathogens and Augments Lipopolysaccharide Activation of Myeloid Cells.The Journal of biological chemistry · 2016Article
- Stool-based biomarkers of interstitial cystitis/bladder pain syndrome.Scientific reports · 2016Article
- Drug and Vaccine Development for the Treatment and Prevention of Urinary Tract Infections.Microbiology spectrum · 2016Review
- Association of O-Antigen Serotype with the Magnitude of Initial Systemic Cytokine Responses and Persistence in the Urinary Tract.Journal of bacteriology · 2016Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The molecular initiators of infection-associated pain are not understood. We recently found that uropathogenic E. coli (UPEC) elicited acute pelvic pain in murine urinary tract infection (UTI). UTI pain was due to E. coli lipopolysaccharide (LPS) and its receptor, TLR4, but pain was not correlated with inflammation. LPS is known to drive inflammation by interactions between the acylated lipid A component and TLR4, but the function of the O-antigen polysaccharide in host responses is unknown. Here, we examined the role of O-antigen in pain using cutaneous hypersensitivity (allodynia) to quantify pelvic pain behavior and using sacral spinal cord excitability to quantify central nervous system manifestations in murine UTI. A UPEC mutant defective for O-antigen biosynthesis induced chronic allodynia that persisted long after clearance of transient infections, but wild type UPEC evoked only acute pain. E. coli strains lacking O-antigen gene clusters had a chronic pain phenotype, and expressing cloned O-antigen gene clusters altered the pain phenotype in a predictable manner. Chronic allodynia was abrogated in TLR4-deficient mice, but inflammatory responses in wild type mice were similar among E. coli strains spanning a wide range of pain phenotypes, suggesting that O-antigen modulates pain independent of inflammation. Spinal cords of mice with chronic allodynia exhibited increased spontaneous firing and compromised short-term depression, consistent with centralized pain. Taken together, these findings suggest that O-antigen functions as a rheostat to modulate LPS-associated pain. These observations have implications for an infectious etiology of chronic pain and evolutionary modification of pathogens to alter host behaviors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.