Evidence map›Paper›PMID 35887098›Full record

ReviewInternational journal of molecular sciences2022

Emerging Concepts in Defective Macrophage Phagocytosis in Cystic Fibrosis.

Devi Jaganathan, Emanuela M Bruscia, Benjamin T Kopp

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. American journal of respiratory cell and molecular biology · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Biofilm-forming strains of P. aeruginosa and S. aureus isolated from cystic fibrosis patients differently affect inflammatory phenotype of macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  12. Immune Response in Cystic Fibrosis: Interplay between the Host and Microbes.International journal of molecular sciences · 2023
    Article
  13. Impact ofInternational journal of molecular sciences · 2022
    Review
  14. Distribution and Characteristics of Bacteria Isolated from Cystic Fibrosis Patients with Pulmonary Exacerbation.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2022
    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.

Devi JaganathanCenter for Microbial Pathogenesis, The Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, OH 43205, USA.
Emanuela M BrusciaDepartment of Pediatrics, Yale University School of Medicine, New Haven, CT 06510, USA.ORCID 0000-0003-2149-4057
Benjamin T KoppCenter for Microbial Pathogenesis, The Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, OH 43205, USA.ORCID 0000-0002-2021-7990
Nationwide Children's Hospital · USYale University · US

Funding

Role of Ezrin in MacrophagesR01AI153422 · NIAID · YALE UNIVERSITY · PI BRUSCIA, EMANUELA MARINA · 2021 to 2025
$3.2M
Pathogenic monocyte response to chronic lung inflammation in cystic fibrosisR01HL157776 · NHLBI · YALE UNIVERSITY · PI BRUSCIA, EMANUELA MARINA · 2022 to 2025
$3.1M
The role of CFTR during macrophage-mediated killing of bacteriaR01HL148171 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI Emanuela Marina Bruscia, Benjamin T Kopp · 2020 to 2026
$2.7M
Resue of CF phagocyte function with CFTR modulator therapyR01HL158747 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI GUGLANI, LOKESH, KOPP, BENJAMIN T · 2022 to 2025
$2.1M
NHLBI NIH HHS R01 HL148171NHLBI NIH HHS R01 HL157776NHLBI NIH HHS R01 HL158747NIAID NIH HHS R01 AI153422
6 · The paper itself

Abstract

Cystic fibrosis (CF) is caused by mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Chronic inflammation and decline in lung function are major reasons for morbidity in CF. Mutant CFTR expressed in phagocytic cells such as macrophages contributes to persistent infection, inflammation, and lung disease in CF. Macrophages play a central role in innate immunity by eliminating pathogenic microbes by a process called phagocytosis. Phagocytosis is required for tissue homeostasis, balancing inflammation, and crosstalk with the adaptive immune system for antigen presentation. This review focused on (1) current understandings of the signaling underlying phagocytic mechanisms; (2) existing evidence for phagocytic dysregulation in CF; and (3) the emerging role of CFTR modulators in influencing CF phagocytic function. Alterations in CF macrophages from receptor initiation to phagosome formation are linked to disease progression in CF. A deeper understanding of macrophages in the context of CFTR and phagocytosis proteins at each step of phagosome formation might contribute to the new therapeutic development of dysregulated innate immunity in CF. Therefore, the review also indicates future areas of research in the context of CFTR and macrophages.

Indexed as

Cystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorHumansInflammationMacrophagesPhagocytosisCystic Fibrosis Transmembrane Conductance Regulatorcystic fibrosisimmune responsemacrophagemicroorganisms

Identifiers

PMID35887098
PMCPMC9319215
OpenAlexW4285495883

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.