Evidence map›Paper›PMID 9819367›Full record

ArticleThe Journal of clinical investigation1998

Apoptosis of human intestinal epithelial cells after bacterial invasion.

J M Kim, L Eckmann, T C Savidge, D C Lowe, T Witthöft, M F Kagnoff

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
6.4field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 314 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Frontiers in cell and developmental biology · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Protective and Anti-Inflammatory Effects of Protegrin-1 onInternational journal of molecular sciences · 2021
    Article
  14. Impact of theToxins · 2020
    Review
  15. Type I interferon remodels lysosome function and modifies intestinal epithelial defense.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  16. Article
  17. Cell death in the gut epithelium and implications for chronic inflammation.Nature reviews. Gastroenterology & hepatology · 2020
    Review
  18. Mechanism of Apoptosis Induced by Curcumin in Colorectal Cancer.International journal of molecular sciences · 2019
    Review
  19. Article
  20. Article

44 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

6 authors at 2 institutions in 2 countries.

J M KimLaboratory of Mucosal Immunology, Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623, USA.
L Eckmann
T C Savidge
D C Lowe
T Witthöft
M F Kagnoff
University of California, San Diego · USBabraham Institute · GB

Funding

TL MOLECULES AND GAMMA-DELTA T CELLSP01DK035108 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KAGNOFF, MARTIN FREDERICK · 1986 to 2013
$19.2M
NIDDK NIH HHS DK35108
6 · The paper itself

Abstract

Epithelial cells that line the human intestinal mucosa are the initial site of host invasion by bacterial pathogens. The studies herein define apoptosis as a new category of intestinal epithelial cell response to bacterial infection. Human colon epithelial cells are shown to undergo apoptosis following infection with invasive enteric pathogens, such as Salmonella or enteroinvasive Escherichia coli. In contrast to the rapid onset of apoptosis seen after bacterial infection of mouse monocyte-macrophage cell lines, the commitment of human intestinal epithelial cell lines to undergo apoptosis is delayed for at least 6 h after bacterial infection, requires bacterial entry and replication, and the ensuing phenotypic expression of apoptosis is delayed for 12-18 h after bacterial entry. TNF-alpha and nitric oxide, which are produced as components of the intestinal epithelial cell proinflammatory program in the early period after bacterial invasion, play an important role in the later induction and regulation of the epithelial cell apoptotic program. Apoptosis in response to bacterial infection may function to delete infected and damaged epithelial cells and restore epithelial cell growth regulation and epithelial integrity that are altered during the course of enteric infection. The delay in onset of epithelial cell apoptosis after bacterial infection may be important both to the host and the invading pathogen since it provides sufficient time for epithelial cells to generate signals important for the activation of mucosal inflammation and concurrently allows invading bacteria time to adapt to the intracellular environment before invading deeper mucosal layers.

Indexed as

ApoptosisAntibodiesBacterial InfectionsBacterial ProteinsCells, CulturedColonEpithelial CellsEscherichia coliHumansIntestinal MucosaNitric OxideNitric Oxide SynthaseSalmonellaTime FactorsTumor Necrosis Factor-alphaAntibodiesBacterial ProteinsNitric OxideNitric Oxide SynthaseTumor Necrosis Factor-alpha

Identifiers

PMID9819367
PMCPMC509131
OpenAlexW2058235525

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.