Evidence map›Paper›PMID 26577570›Full record

ArticleMucosal immunology2016

Restoring cigarette smoke-induced impairment of efferocytosis in alveolar macrophages.

R Subramaniam, S Mukherjee, H Chen, S Keshava, P Neuenschwander, H Shams

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Efferocytosis in Homeostasis.Advances in experimental medicine and biology · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Ras and Rab Interactor 3: From Cellular Mechanisms to Human Diseases.Frontiers in cell and developmental biology · 2022
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. 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

6 authors at 2 institutions in 1 country.

R SubramaniamCenter for Pulmonary and Infectious Diseases Control (CPIDC), The University of Texas Health Science Center at Tyler, Tyler, Texas, USA.
S MukherjeeCenter for Pulmonary and Infectious Diseases Control (CPIDC), The University of Texas Health Science Center at Tyler, Tyler, Texas, USA.
H ChenCenter for Pulmonary and Infectious Diseases Control (CPIDC), The University of Texas Health Science Center at Tyler, Tyler, Texas, USA.
S KeshavaDepartment of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, Tyler, Texas, USA.
P NeuenschwanderBiomedical research, The University of Texas Health Science Center at Tyler, Tyler, Texas, USA.
H ShamsCenter for Pulmonary and Infectious Diseases Control (CPIDC), The University of Texas Health Science Center at Tyler, Tyler, Texas, USA.
The University of Texas Health Science Center at Tyler · USMassachusetts General Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cigarette smoke has been associated with susceptibility to different pulmonary and airway diseases. Impaired alveolar macrophages (AMs) that are major phagocytes in the lung have been associated with patients with airway diseases and active smokers. In the current report, we show that exposure to second-hand cigarette smoke (SHS) significantly reduced efferocytosis in vivo. More importantly, delivery of recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF) to the alveolar space restored and refurbished the efferocytosis capability of AMs. Exposure to SHS significantly reduced expression of CD16/32 on AMs, and treatment with GM-CSF not only restored but also significantly increased the expression of CD16/32 on AMs. GM-CSF treatment increased uptake and digestion/removal of apoptotic cells by AMs. The latter was attributed to increased expression of Rab5 and Rab7. Increased efferocytosis of AMs was also tested in a disease condition. AMs from GM-CSF-treated, influenza-infected, SHS-exposed mice showed significantly better efferocytosis activity, and mice had significantly less morbidity compared with phosphate-buffered saline-treated group. GM-CSF-treated mice had increased amphiregulin levels in the lungs, which in addition to efferocytosis of AMs may have attributed to their protection against influenza. These results will have great implications for developing therapeutic approaches by harnessing mucosal innate immunity to treat lung and airway diseases and protect against pneumonia.

Indexed as

AmphiregulinAnimalsApoptosisCells, CulturedGranulocyte-Macrophage Colony-Stimulating FactorImmunity, InnateLungMacrophages, AlveolarMiceMice, Inbred C57BLOrthomyxoviridaeOrthomyxoviridae InfectionsPhagocytosisrab5 GTP-Binding Proteinsrab7 GTP-Binding Proteinsrab GTP-Binding ProteinsAmphiregulinGranulocyte-Macrophage Colony-Stimulating Factorrab5 GTP-Binding Proteinsrab7 GTP-Binding Proteinsrab7 GTP-binding proteins, mouserab GTP-Binding ProteinsTobacco Smoke Pollution

Identifiers

PMID26577570
OpenAlexW2414018723

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.