ArticleJournal of inflammation (London, England)2023
Inhibition of COX-2 signaling favors E. coli during urinary tract infection.
Article in Journal of inflammation (London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Harnessing pro-inflammatory and immunopathologic immune responses in urinary tract infections for vaccine development: it's all about a balance.Frontiers in immunology · 2026Review
- Urinary tract infections: pathogenesis, host susceptibility and emerging therapeutics.Nature reviews. Microbiology · 2025Review
- Synthetic antimicrobial peptide LD4-PP protects the host againstFrontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo avoid the overuse of antibiotics, non-steroidal anti-inflammatory drugs (NSAIDs), acting via cyclooxygenase (COX) inhibition, have been used to reduce pain and as an alternative treatment for uncomplicated urinary tract infections (UTIs). However, clinical studies evaluating NSAIDs versus antibiotics have reported an increased risk of acute pyelonephritis. Therefore, we hypothesized that COX inhibition could compromise the innate immune response and contribute to complications in patients with uncomplicated UTI.
resultsWe here demonstrate that in particular COX-2 inhibition led to decreased expression of the antimicrobial peptides psoriasin and human β-defensin-2 in human uroepithelial cells. Psoriasin expression was altered in neutrophils and macrophages. COX-2 inhibition also had impact on the inflammasome mediated IL-1β expression in response to uroepithelial E. coli infection. Further, COX-2 inhibition downregulated free radicals and the epithelial barrier protein claudin 1, favoring infectivity. In addition, conditioned media from COX-2 inhibited uroepithelial cells infected with E. coli failed to activate macrophages.
conclusionsTaken together, our data suggests an adverse innate immune effect of COX-2 inhibition on uroepithelial cells during UTI.
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Registered trials
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