Evidence map›Paper›PMID 23311949›Full record

ArticleCellular microbiology2013

Cryptosporidium parvum scavenges LDL-derived cholesterol and micellar cholesterol internalized into enterocytes.

Karen Ehrenman, Jane W Wanyiri, Najma Bhat, Honorine D Ward, Isabelle Coppens

Open access · bronzeAbstract read
In one paragraph

Article in Cellular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Frontiers in cellular and infection microbiology · 2026
    Article
  2. Article
  3. Article
  4. Novel Insights Into Sterol Uptake and Intracellular Cholesterol Trafficking DuringFrontiers in cellular and infection microbiology · 2022
    Article
  5. Article
  6. Ezetimibe blocksParasitology · 2021
    Article
  7. P-Glycoprotein Inhibitors Differently AffectPathogens (Basel, Switzerland) · 2021
    Article
  8. Article
  9. Frontiers in cellular and infection microbiology · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Isoprenoid metabolism in apicomplexan parasites.Current clinical microbiology reports · 2014
    Article
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

5 authors at 2 institutions in 1 country.

Karen EhrenmanDepartment of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Jane W Wanyiri
Najma Bhat
Honorine D Ward
Isabelle Coppens
Johns Hopkins University · USTufts Medical Center · US

Funding

Targeting of host vesicles to the vacuole of Toxoplasma and lipid cargo sortingR01AI060767 · NIAID · JOHNS HOPKINS UNIVERSITY · PI COPPENS, ISABELLE · 2004 to 2020
$5.1M
Cholesterol Uptake by CryptosporidiumR21AI081562 · NIAID · JOHNS HOPKINS UNIVERSITY · PI COPPENS, ISABELLE · 2009 to 2010
$449k
NIAID NIH HHS AI081562NIAID NIH HHS R01 AI060767NIAID NIH HHS R21 AI081562
6 · The paper itself

Abstract

Cryptosporidium spp. are responsible for devastating diarrhoea in immunodeficient individuals. In the intestinal tract, the developmental stages of the parasite are confined to the apical surfaces of epithelial cells. Upon invasion, Cryptosporidium incorporates the microvillous membrane of the enterocyte to form the parasitophorous vacuole (PV) and sequesters itself from the host cytoplasm by rearranging the host cytoskeleton. Cryptosporidium parvum has minimal anabolic capabilities and relies on transporters and salvage pathways to meet its basic metabolic requirements. The cholesterol salvage pathway is crucial for the development of protozoan parasites. In this study, we have examined the sources of cholesterol from C. parvum infecting enterocytes. We illustrated that the intracellular stages of Cryptosporidium as well as the oocysts shed by the host, contain cholesterol. Incubation of infected enterocytes in lipoprotein-free medium impairs parasite development and results in substantial decrease in cholesterol content associated with the PV. Among lipoproteins, LDL constitutes an important source of cholesterol for Cryptosporidium. Dietary cholesterol incorporated into micelles is internalized into enterocytes by the NPC1L1 transporter. We showed that C. parvum also obtains cholesterol from micelles in enterocytes.Pharmacological blockade of NPC1L1 function by ezetimibe or moderate downregulation of NPC1L1 expression decreases parasite infectivity. These observations indicate that, despite its dual sequestration from the intestinal lumen and the host cytoplasm, C. parvum can, in fact, obtain cholesterol both from the gut's lumen and the host cell. This study highlights the evolutionary advantages for epicellular pathogens to access to nutrients from the outside and inside of the host cell.

Indexed as

Cell LineCholesterol, LDLCryptosporidium parvumEnterocytesHumansMembrane ProteinsMembrane Transport ProteinsMicroscopyModels, BiologicalCholesterol, LDLMembrane ProteinsMembrane Transport ProteinsNPC1L1 protein, human

Identifiers

PMID23311949
PMCPMC3644335
OpenAlexW1930915198

What OpenQuestion holds

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Registered trials

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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.