Evidence map›Paper›PMID 20225955›Full record

ArticleThe Journal of infectious diseases2010

Host-pathogen interactions mediating pain of urinary tract infection.

Charles N Rudick, Benjamin K Billips, Vladimir I Pavlov, Ryan E Yaggie, Anthony J Schaeffer, David J Klumpp

Abstract read
In one paragraph

Article in The Journal of infectious diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 60 citations in OpenAlex.

  1. Bladder mucosal afferents detect UTI and aid pathogen clearance.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Bladder infection with uropathogenicAmerican journal of physiology. Renal physiology · 2022
    Article
  10. Article
  11. Microbes and pain.PLoS pathogens · 2021
    Review
  12. Review
  13. Pain and immunity: implications for host defence.Nature reviews. Immunology · 2019
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Infection, Pain, and Itch.Neuroscience bulletin · 2018
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Charles N RudickDepartment of Urology, Feinberg School of Medicine Northwestern University, Chicago, Illinois, USA.
Benjamin K Billips
Vladimir I Pavlov
Ryan E Yaggie
Anthony J Schaeffer
David J Klumpp
Northwestern University · US

Funding

Role of CNS in Modulation of Pelvic Pain SyndromeU01DK082342 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KLUMPP, DAVID J · 2008 to 2021
$10.5M
Basic Science Training Grant in UrologyT32DK062716 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KLUMPP, DAVID J · 2003 to 2020
$2.0M
ROLE OF TNF IN BLADDER INFLAMMATIONR01DK066112 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KLUMPP, DAVID J · 2003 to 2010
$1.8M
NIDDK NIH HHS R01 DK066112NIDDK NIH HHS R01DK066112NIDDK NIH HHS T32 DK062716NIDDK NIH HHS T32DK062716-05NIDDK NIH HHS U01 DK082342PHS HHS U09DKO8234
6 · The paper itself

Abstract

backgroundPelvic pain is a major component of the morbidity associated with urinary tract infection (UTI), yet the molecular mechanisms underlying UTI-induced pain remain unknown. UTI pain mechanisms probably contrast with the clinical condition of asymptomatic bacteriuria (ASB), characterized by significant bacterial loads without lack symptoms.

methodsA murine UTI model was used to compare pelvic pain behavior elicited by infection with uropathogenic Escherichia coli strain NU14 and ASB strain 83972.

resultsNU14-infected mice exhibited pelvic pain, whereas mice infected with 83972 did not exhibit pain, similar to patients infected with 83972. NU14-induced pain was not dependent on mast cells, not correlated with bacterial colonization or urinary neutrophils. UTI pain was not influenced by expression of type 1 pili, the bacterial adhesive appendages that induce urothelial apoptosis. However, purified NU14 lipopolysaccharide (LPS) induced Toll-like receptor 4 (TLR4)-dependent pain, whereas 83972 LPS induced no pain. Indeed, 83972 LPS attenuated the pain of NU14 infection, suggesting therapeutic potential.

conclusionsThese data suggest a novel mechanism of infection-associated pain that is dependent on TLR4 yet independent of inflammation. Clinically, these findings also provide the rational for probiotic therapies that would minimize the symptoms of infection without reliance on empirical therapies that contribute to antimicrobial resistance.

Indexed as

AnimalsCarrier StateEscherichia coli InfectionsFemaleHost-Pathogen InteractionsLipopolysaccharidesMacrophagesMast CellsMiceMice, Inbred C3HMice, Inbred C57BLPelvic PainReceptors, ImmunologicToll-Like Receptor 4Urinary Bladder DiseasesUrinary Tract Infectionsfimbriae receptor, type 1LipopolysaccharidesReceptors, ImmunologicTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID20225955
PMCPMC2841043
OpenAlexW2131686092

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.