Evidence map›Paper›PMID 27002654›Full record

ArticleAutophagy2016

Ferritinophagy drives uropathogenic Escherichia coli persistence in bladder epithelial cells.

Kyle A Bauckman, Indira U Mysorekar

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Guideline
  2. Article
  3. Overview of Ferroptosis in Cadmium Toxicity.Biological trace element research · 2026
    Review
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5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Kyle A Bauckmana Departments of Obstetrics & Gynecology, Washington University School of Medicine , St. Louis , MO , USA.
Indira U Mysorekara Departments of Obstetrics & Gynecology, Washington University School of Medicine , St. Louis , MO , USA.
Washington University in St. Louis · US

Funding

Training in Reproductive SciencesT32HD049305 · NICHD · WASHINGTON UNIVERSITY · PI MOLEY, KELLE H · 2005 to 2015
$1.9M
ATG16L1 AND MOLECULAR REGULATION OF BACTERIAL PERSISTENCER01DK100644 · NIDDK · WASHINGTON UNIVERSITY · PI MYSOREKAR, INDIRA U · 2013 to 2017
$1.7M
INTERLEUKIN-6 AND AGING: IMPACT ON IMMUNE DEFENSE AND TISSUE REPAIR IN URINARY BLADDERR01AG052494 · NIA · WASHINGTON UNIVERSITY · PI LOWDER, JERRY LANE, MYSOREKAR, INDIRA U · 2016 to 2020
$1.6M
NIA NIH HHS R01 AG052494NICHD NIH HHS T32 HD049305NIDDK NIH HHS R01 DK100644
6 · The paper itself

Abstract

Autophagy is a cellular recycling pathway, which in many cases, protects host cells from infections by degrading pathogens. However, uropathogenic Escherichia coli (UPEC), the predominant cause of urinary tract infections (UTIs), persist within the urinary tract epithelium (urothelium) by forming reservoirs within autophagosomes. Iron is a critical nutrient for both host and pathogen, and regulation of iron availability is a key host defense against pathogens. Iron homeostasis depends on the shuttling of iron-bound ferritin to the lysosome for recycling, a process termed ferritinophagy (a form of selective autophagy). Here, we demonstrate for the first time that UPEC shuttles with ferritin-bound iron into the autophagosomal and lysosomal compartments within the urothelium. Iron overload in urothelial cells induces ferritinophagy in an NCOA4-dependent manner causing increased iron availability for UPEC, triggering bacterial overproliferation and host cell death. Addition of even moderate levels of iron is sufficient to increase and prolong bacterial burden. Furthermore, we show that lysosomal damage due to iron overload is the specific mechanism causing host cell death. Significantly, we demonstrate that host cell death and bacterial burden can be reversed by inhibition of autophagy or inhibition of iron-regulatory proteins, or chelation of iron. Together, our findings suggest that UPEC persist in host cells by taking advantage of ferritinophagy. Thus, modulation of iron levels in the bladder may provide a therapeutic avenue to controlling UPEC persistence, epithelial cell death, and recurrent UTIs.

Indexed as

Uropathogenic Escherichia coliAutophagyEpithelial CellsEscherichia coli InfectionsHumansIronLysosomesUrinary BladderUrinary Tract InfectionsIrondeferoxamine (DFO)E. coliferric ammonium citrate (FAC)ferrumNCOA4UPECurinary tract infections (UTIs)

Identifiers

PMID27002654
PMCPMC4854542
OpenAlexW2309889647

What OpenQuestion holds

Textmetadata
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.