Evidence map›Paper›PMID 16177360›Full record

ArticleInfection and immunity2005

Influence of cystic fibrosis transmembrane conductance regulator on gene expression in response to Pseudomonas aeruginosa infection of human bronchial epithelial cells.

Nina Reiniger, Jeffrey K Ichikawa, Gerald B Pier

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Newborn Cystic Fibrosis Pigs Have a Blunted Early Response to an Inflammatory Stimulus.American journal of respiratory and critical care medicine · 2016
    Article
  7. Article
  8. Breaking barriers. New insights into airway epithelial barrier function in health and disease.American journal of respiratory cell and molecular biology · 2014
    Review
  9. Article
  10. Article
  11. Article
  12. Does the F508-CFTR mutation induce a proinflammatory response in human airway epithelial cells?American journal of physiology. Lung cellular and molecular physiology · 2012
    Article
  13. Entry of Burkholderia organisms into respiratory epithelium: CFTR, microfilament and microtubule dependence.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2010
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

3 authors at 2 institutions in 1 country.

Nina ReinigerChanning Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
Jeffrey K Ichikawa
Gerald B Pier
Brigham and Women's Hospital · USHarvard University · US

Funding

CFTR AND INFECTION OF CYSTIC FIBROSIS PATIENTSR01HL058398 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI PIER, GERALD B · 1997 to 2009
$3.4M
Colorimetric Substrates of SAP2 for Vaginal CandidiasisR43AI058398 · NIAID · GRYPHUS DIAGNOSTICS, LLC · PI JOHNSON, STEPHEN C · 2004 to 2004
$80k
NHLBI NIH HHS R01 HL058398NIAID NIH HHS AI HL58398
6 · The paper itself

Abstract

Chronic lung infection by Pseudomonas aeruginosa causes significant morbidity in cystic fibrosis patients initiated by the failure of innate immune responses. We used microarray analysis and real-time PCR to detect transcriptional changes associated with cytokine production in isogenic bronchial epithelial cell lines with either wild-type (WT) or mutant cystic fibrosis transmembrane conductance regulator (CFTR) in response to P. aeruginosa infection. The transcription of four NF-kappaB-regulated cytokine genes was maximal in the presence of WT CFTR: the interleukin-8 (IL-8), IL-6, CXCL1, and intracellular adhesion molecule 1 (ICAM-1) genes. Analysis of protein expression in two cell lines paired for wild-type and mutant CFTR with three P. aeruginosa strains showed IL-6 and IL-8 expressions were consistently enhanced by the presence of WT CFTR in both cell lines with all three strains of P. aeruginosa, although some strains gave small IL-8 increases in cells with mutant CFTR. CXCL1 production showed consistent enhancement in cells with WT CFTR using all three bacterial strains in one cell line, whereas in the other cell line, CXCL1 showed a significant increase in cells with either WT or mutant CFTR. ICAM-1 was unchanged at the protein level in one of the cell lines but did show mild enhancement with WT CFTR in the other cell pair. Inhibitions of NF-kappaB prior to infection indicated differing degrees of dependence on NF-kappaB for production of the cytokines, contingent on the cell line. Cytokine effectors of innate immunity to P. aeruginosa were found to be positively influenced by the presence of WT CFTR, indicating a role in resistance to P. aeruginosa infection.

Indexed as

Pseudomonas aeruginosaBronchiCell LineCystic Fibrosis Transmembrane Conductance RegulatorCytokinesEpithelial CellsGene ExpressionHumansImmunity, InnateMutationNF-kappa BOligonucleotide Array Sequence AnalysisPneumonia, BacterialPseudomonas InfectionsCystic Fibrosis Transmembrane Conductance RegulatorCytokinesNF-kappa B

Identifiers

PMID16177360
PMCPMC1230967
OpenAlexW2164448670

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.