Evidence map›Paper›PMID 30337926›Full record

ArticleFrontiers in immunology2018

Suppression of Neutrophil Antimicrobial Functions by Total Particulate Matter From Cigarette Smoke.

Yao Zhang, Shuo Geng, G L Prasad, Liwu Li

Abstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Role of Neutrophils on the Ocular Surface.International journal of molecular sciences · 2021
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. No smoke without fire: the impact of cigarette smoking on the immune control of tuberculosis.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  7. Particulate matter (PMScientific reports · 2022
    Article
  8. Review
  9. Air pollution by NOScientific reports · 2020
    Article
  10. Review
  11. Article
  12. Article
  13. 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

4 authors.

Yao ZhangDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA, United States.
Shuo GengDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA, United States.
G L PrasadRAI Services Company, Winston-Salem, NC, United States.
Liwu LiDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic cigarette smoking is widely known to alter immune functions and compromise host defense against microbial infection. Neutrophils play an essential role in the immune defense against microbial pathogens and also participate in the development of the inflammatory responses. However, there is limited information about the effects of cigarette smoking on neutrophil response. In this study, cultured bone marrow neutrophils were exposed to total particulate matter (TPM) from cigarette smoke. We found that TPM not only reduced LPS-induced TNFα production, but also suppressed neutrophil bactericidal activity. We also observed that TPM priming reduced the expression of NADPH oxidase component gp91 and iNOS, molecules important for bacterial killing. Mechanistically, we documented that TPM-primed neutrophils have reduced STAT1 activation following subsequent LPS challenge. STAT1 is a key transcription factor responsible for the expression of inflammatory genes as well as gp91 and iNOS. Collectively, reduced STAT1 activation and reduced NADPH oxidase/iNOS may potentially explain the compromised anti-microbial function of TPM-programmed neutrophils. Taken together, our findings reveal that the key innate immune neutrophil is subject to reprogramming by smoking to adopt an immune-suppressed state, potentially responsible for chronic smoking-mediated immunosuppression.

Indexed as

AnimalsAnti-Infective AgentsCells, CulturedGene ExpressionImmune ToleranceLipopolysaccharidesMice, Inbred C57BLNADPH OxidasesNeutrophilsNicotianaNitric Oxide Synthase Type IIParticulate MatterSmokeSTAT1 Transcription FactorAnti-Infective AgentsLipopolysaccharidesNADPH OxidasesNitric Oxide Synthase Type IIParticulate MatterSmokeSTAT1 Transcription Factorimmune-modulationinflammationNADPH oxidaseneutrophil programmingTPM

Identifiers

PMID30337926
PMCPMC6180193

What OpenQuestion holds

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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.