Evidence map›Paper›PMID 32522666›Full record

ArticleImmunology letters2020

How nicotine can inhibit cytokine storm in the lungs and prevent or lessen the severity of COVID-19 infection?

Malgorzata Kloc, Rafik M Ghobrial, Jacek Z Kubiak

Open access · greenAbstract readLetter
In one paragraph

Article in Immunology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Cholinergic dysfunction in COVID-19: frantic search and hoping for the best.Naunyn-Schmiedeberg's archives of pharmacology · 2023
    Review
  10. Article
  11. An experimental test of the nicotinic hypothesis of COVID-19.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Article
  13. Review
  14. Inflammatory reflex disruption in COVID-19.Clinical & experimental neuroimmunology · 2022
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  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 3 countries.

Malgorzata KlocThe Houston Methodist Research Institute, Houston, Texas 77030, USA; The Houston Methodist Hospital, Department of Surgery, Houston, Texas, USA; The University of Texas, M.D. Anderson Cancer Center, Department of Genetics, Houston Texas, USA. Electronic address: mkloc@houstonmethodist.org.
Rafik M GhobrialThe Houston Methodist Research Institute, Houston, Texas 77030, USA; The Houston Methodist Hospital, Department of Surgery, Houston, Texas, USA.
Jacek Z KubiakLaboratory of Regenerative Medicine and Cell Biology, Military Institute of Hygiene and Epidemiology (WIHE), Warsaw, Poland; UnivRennes, UMR 6290, CNRS, Institute of Genetics and Development of Rennes, Cell Cycle Group, Faculty of Medicine, Rennes, France. Electronic address: jacek.kubiak@univ-rennes1.fr.
Methodist Hospital · USWojskowy Instytut Higieny i Epidemiologii · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Statistical surveys of COVID-19 patients indicate, against all common logic, that people who smoke are less prone to the infection and/or exhibit less severe respiratory symptoms than non-smokers. This suggests that nicotine may have some preventive or modulatory effect on the inflammatory response in the lungs. Because it is known that the response to, and resolution of the SARS-CoV-2 infection depends mainly on the lung macrophages, we discuss the recent scientific findings, which may explain why and how nicotine may modulate lung macrophage response during COVID-19 infection.

Indexed as

SmokersAdministration, Inhalationalpha7 Nicotinic Acetylcholine ReceptorAnti-Inflammatory AgentsBetacoronavirusCoronavirus InfectionsCOVID-19Cytokine Release SyndromeCytokinesHost-Pathogen InteractionsHumansLungMacrophagesNicotineNicotinic AgonistsPandemicsalpha7 Nicotinic Acetylcholine ReceptorAnti-Inflammatory AgentsChrna7 protein, humanCytokinesNicotineNicotinic AgonistsReceptors, NicotinicAcute respiratory distress syndrome - ARDSCOVID-19CytokinesCytokine stormInflammationLungsMacrophagesNicotineSARS-CoV-2α4/α7 Nicotinic Ach receptors - nAChRs

Identifiers

PMID32522666
PMCPMC7836994
OpenAlexW3033859684

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.