ArticleNature communications2025
Two-component system GrpP/GrpQ promotes pathogenicity of uropathogenic Escherichia coli CFT073 by upregulating type 1 fimbria.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed.
- Identification of a mechanical signaling pathway activating type 1 fimbriae via a ZraSR two-component system in neonatal meningitis-associatedVirulence · 2026Article
- RstAB activates type 1 fimbriae to promote uropathogeniciScience · 2026Article
- A cold-responsiveApplied and environmental microbiology · 2026Article
- The IrlS2-IrlR2 two-component system is a global regulator of biofilm formation, stress adaptation, and virulence inmSphere · 2026Article
- Catabolism of serine enantiomers represses enterohemorrhagicProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Chimeric vaccine based on Iraqi HLA alleles against a predominant localFrontiers in immunology · 2026Article
- The BaeS/BaeR two-component system enhancesFrontiers in cellular and infection microbiology · 2026Article
- Maximizing bacterial survival: integrating sense-and-respond and bet-hedging mechanisms.Trends in microbiology · 2025Review
- Article
- Cranberry-Derived Phenolic Compounds Contribute to the Inhibition of FimH-MediatedAntibiotics (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Uropathogenic Escherichia coli (UPEC) is a major cause of urinary tract infections (UTIs). Invasion into bladder epithelial cells (BECs) on the bladder luminal surface via type 1 fimbria is the first critical step in UPEC infection. Although type 1 fimbria expression increases during UPEC invasion of BECs, the underlying regulatory mechanisms remain poorly understood. This study reported a previously uncharacterized two-component system (TCS) GrpP/GrpQ that directly activates type 1 fimbria expression to promote UPEC invasion and therefore pathogenicity in response to D-serine present in the host urine. grpP/grpQ mutation severely impaired UPEC invasion of BECs and decreased the bacterial burden and formation of intracellular bacterial communities in mouse bladders during acute UTI. grpP/grpQ is widely present in UPEC genomes but rarely in other E. coli genomes, suggesting that this TCS specifically contributes to UPEC evolution. This study revealed a new pathway for virulence activation in response to host cues, providing further insight into UPEC pathogenesis and a promising target for UTI treatment.
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Registered trials
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