Evidence map›Paper›PMID 21625641›Full record

ArticlePloS one2011

Dysfunctional CFTR alters the bactericidal activity of human macrophages against Pseudomonas aeruginosa.

Paola Del Porto, Noemi Cifani, Simone Guarnieri, Enea Gino Di Domenico, Maria A Mariggiò, Francesca Spadaro, Silvia Guglietta, Marco Anile, Federico Venuta, Serena Quattrucci and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
7.5field-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

101 citing papers in PubMed, 163 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The Challenges of Detecting Neutrophil CFTR.Journal of innate immunity · 2026
    Review
  5. Article
  6. Article
  7. Zebrafish (International journal of molecular sciences · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. CFTR is required for zinc-mediated antibacterial defense in human macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

41 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

11 authors at 5 institutions in 1 country.

Paola Del PortoDepartment of Biology and Biotechnology Charles Darwin, Sapienza University, Rome, Italy. delporto@uniroma1.it
Noemi Cifani
Simone Guarnieri
Enea Gino Di Domenico
Maria A Mariggiò
Francesca Spadaro
Silvia Guglietta
Marco Anile
Federico Venuta
Serena Quattrucci
Fiorentina Ascenzioni
Sapienza University of Rome · ITPoliclinico Umberto I · ITUniversity of Chieti-Pescara · ITIstituto Superiore di Sanità · ITRegione Lazio

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation of the lung, as a consequence of persistent bacterial infections by several opportunistic pathogens represents the main cause of mortality and morbidity in cystic fibrosis (CF) patients. Mechanisms leading to increased susceptibility to bacterial infections in CF are not completely known, although the involvement of cystic fibrosis transmembrane conductance regulator (CFTR) in microbicidal functions of macrophages is emerging. Tissue macrophages differentiate in situ from infiltrating monocytes, additionally, mature macrophages from different tissues, although having a number of common activities, exhibit variation in some molecular and cellular functions. In order to highlight possible intrinsic macrophage defects due to CFTR dysfunction, we have focused our attention on in vitro differentiated macrophages from human peripheral blood monocytes. Here we report on the contribution of CFTR in the bactericidal activity against Pseudomonas aeruginosa of monocyte derived human macrophages. At first, by real time PCR, immunofluorescence and patch clamp recordings we demonstrated that CFTR is expressed and is mainly localized to surface plasma membranes of human monocyte derived macrophages (MDM) where it acts as a cAMP-dependent chloride channel. Next, we evaluated the bactericidal activity of P. aeruginosa infected macrophages from healthy donors and CF patients by antibiotic protection assays. Our results demonstrate that control and CF macrophages do not differ in the phagocytic activity when infected with P. aeruginosa. Rather, although a reduction of intracellular live bacteria was detected in both non-CF and CF cells, the percentage of surviving bacteria was significantly higher in CF cells. These findings further support the role of CFTR in the fundamental functions of innate immune cells including eradication of bacterial infections by macrophages.

Indexed as

AdolescentAdultCystic Fibrosis Transmembrane Conductance RegulatorFemaleHumansMacrophagesMaleMicroscopy, ConfocalMicroscopy, FluorescenceMiddle AgedPseudomonas aeruginosaCystic Fibrosis Transmembrane Conductance Regulator

Identifiers

PMID21625641
PMCPMC3097223
OpenAlexW1991964554

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.