Evidence map›Paper›PMID 31631328›Full record

ArticleClinical and experimental immunology2020

Nicotine modulates molecules of the innate immune response in epithelial cells and macrophages during infection with M. tuberculosis.

C E Valdez-Miramontes, L A Trejo Martínez, F Torres-Juárez, A Rodríguez Carlos, S P Marin-Luévano, J P de Haro-Acosta, J A Enciso-Moreno, B Rivas-Santiago

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-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

29 citing papers in PubMed, 48 citations in OpenAlex.

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  13. Nicotinic regulation of microglia: potential contributions to addiction.Journal of neural transmission (Vienna, Austria : 1996) · 2024
    Review
  14. Nicotinic receptors in airway disease.American journal of physiology. Lung cellular and molecular physiology · 2024
    Review
  15. Review
  16. Article
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  18. The controversial effect of smoking and nicotine in SARS-CoV-2 infection.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023
    Review
  19. Review
  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

8 authors at 2 institutions in 1 country.

C E Valdez-MiramontesMedical Research Unit-Zacatecas, Mexican Institute for Social Security-IMSS, Zacatecas, Mexico.
L A Trejo MartínezMedical Research Unit-Zacatecas, Mexican Institute for Social Security-IMSS, Zacatecas, Mexico.
F Torres-JuárezMedical Research Unit-Zacatecas, Mexican Institute for Social Security-IMSS, Zacatecas, Mexico.
A Rodríguez CarlosMedical Research Unit-Zacatecas, Mexican Institute for Social Security-IMSS, Zacatecas, Mexico.
S P Marin-LuévanoMedical Research Unit-Zacatecas, Mexican Institute for Social Security-IMSS, Zacatecas, Mexico.
J P de Haro-AcostaMedical Research Unit-Zacatecas, Mexican Institute for Social Security-IMSS, Zacatecas, Mexico.
J A Enciso-MorenoMedical Research Unit-Zacatecas, Mexican Institute for Social Security-IMSS, Zacatecas, Mexico.
B Rivas-SantiagoMedical Research Unit-Zacatecas, Mexican Institute for Social Security-IMSS, Zacatecas, Mexico.ORCID 0000-0002-1521-1519
Institute for Scientific and Technological Research · MXUniversidad Autónoma de Zacatecas "Francisco García Salinas" · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Smoking increases susceptibility to becoming infected with and developing tuberculosis. Among the components of cigarette smoke, nicotine has been identified as the main immunomodulatory molecule; however, its effect on the innate immune system is unknown. In the present study, the effect of nicotine on molecules of the innate immune system was evaluated. Lung epithelial cells and macrophages were infected with Mycobacterium tuberculosis (Mtb) and/or treated with nicotine. The results show that nicotine alone decreases the expression of the Toll-like receptors (TLR)-2, TLR-4 and NOD-2 in all three cell types, as well as the production of the SP-D surfactant protein in type II pneumocytes. Moreover, it was observed that nicotine decreases the production of interleukin (IL)-6 and C-C chemokine ligand (CCL)5 during Mtb infection in epithelial cells (EpCs), whereas in macrophages derived from human monocytes (MDMs) there is a decrease in IL-8, IL-6, tumor necrosis factor (TNF)-α, IL-10, CCL2, C-X-C chemokine ligand (CXCL)9 and CXCL10 only during infection with Mtb. Although modulation of the expression of cytokines and chemokines appears to be partially mediated by the nicotinic acetylcholine receptor α7, blocking this receptor found no effect on the expression of receptors and SP-D. In summary, it was found that nicotine modulates the expression of innate immunity molecules necessary for the defense against tuberculosis.

Indexed as

A549 CellsAlveolar Epithelial CellsCytokinesGene Expression RegulationHumansImmunity, InnateMacrophagesMycobacterium tuberculosisNicotineNod2 Signaling Adaptor ProteinToll-Like Receptor 2Toll-Like Receptor 4Tuberculosis, PulmonaryCytokinesNicotineNOD2 protein, humanNod2 Signaling Adaptor ProteinTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4cigarette smokeepithelial cellsmacrophagesMycobacterium tuberculosisnicotine

Identifiers

PMID31631328
PMCPMC6954679
OpenAlexW2981855313

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.