Evidence map›Paper›PMID 18519556›Full record

ArticleInfection and immunity2008

Inhibition of apoptosis in Cryptosporidium parvum-infected intestinal epithelial cells is dependent on survivin.

Jin Liu, Shinichiro Enomoto, Cheryl A Lancto, Mitchell S Abrahamsen, Mark S Rutherford

Abstract read
In one paragraph

Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

26 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. LncRNA BACE1-AS delays the propagation ofMicrobiology spectrum · 2025
    Article
  6. Review
  7. mBio · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Early immune and host cell responses toFrontiers in parasitology · 2023
    Article
  12. Apoptotic changes in the intestinal epithelium ofJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2022
    Article
  13. Article
  14. International journal of environmental research and public health · 2022
    Article
  15. IsFood and waterborne parasitology · 2022
    Article
  16. Management of cell death in parasitic infections.Seminars in immunopathology · 2021
    Review
  17. Frontiers in veterinary science · 2021
    Article
  18. Review
  19. Frontiers in microbiology · 2020
    Article
  20. Review
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 1 institution in 1 country.

Jin LiuDepartment of Veterinary and Biomedical Sciences, University of Minnesota, 1988 Fitch Ave, no. 295, St. Paul, MN 55108, USA.
Shinichiro Enomoto
Cheryl A Lancto
Mitchell S Abrahamsen
Mark S Rutherford
University of Minnesota · US

Funding

Host specificity of Cryptosporidium gene expressionR01AI065246 · NIAID · UNIVERSITY OF MINNESOTA · PI RUTHERFORD, MARK STEPHEN · 2006 to 2009
$1.9M
NIAID NIH HHS R01 AI065246NIAID NIH HHS R01-AI065246-02
6 · The paper itself

Abstract

Cryptosporidium parvum is an obligate intracellular protozoan capable of causing severe diarrheal disease in a wide variety of mammals, including humans. C. parvum infection has been associated with induction of apoptosis in exposed epithelial cells, and we now demonstrate that apoptosis is restricted to a subset of cells actively infected with C. parvum. Approximately 20% of the infected cells underwent apoptosis within 48 h of infection, suggesting that the majority of the infected cells are rescued from apoptosis. C. parvum infection resulted in low-level activation of multiple members of the caspase family, including caspase-2, -3, -4, -6, -8, and -9. The kinetics of caspase activation correlated with apoptosis over a 48-h time course. Pan caspase inhibitors reduced apoptosis of epithelial cells infected by C. parvum. Furthermore, C. parvum infection inhibited staurosporine-induced apoptosis and caspase-3/7 activation at 24 h and 48 h. Infection with C. parvum led to upregulation of genes encoding inhibitors of apoptosis proteins (IAPs), including c-IAP1, c-IAP2, XIAP, and survivin. Knockdown of survivin gene expression, but not that of c-IAP1, c-IAP2, or XIAP expression, increased caspase-3/7 activity as well as apoptosis of infected cells and decreased C. parvum 18S rRNA levels. These data suggest that the apoptotic response of infected intestinal epithelial cells is actively suppressed by C. parvum via upregulation of survivin, favoring parasite infection.

Indexed as

ApoptosisCaspase InhibitorsAnimalsCell LineCryptosporidium parvumEpithelial CellsGene SilencingHumansInhibitor of Apoptosis ProteinsIntestinal MucosaMicrotubule-Associated ProteinsNeoplasm ProteinsSurvivinBIRC5 protein, humanCaspase InhibitorsInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsNeoplasm ProteinsSurvivin

Identifiers

PMID18519556
PMCPMC2493198
OpenAlexW2139471821

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.