Evidence map›Paper›PMID 34155778›Full record

ArticleJournal of cellular and molecular medicine2021

Smoking increases oral mucosa susceptibility to Candida albicans infection via the Nrf2 pathway: In vitro and animal studies.

Pei Ye, Wei Chen, Fan Huang, Qin Liu, Ya-Nan Zhu, Xiang Wang, Xiao-Dong Han, Wen-Mei Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

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  3. International journal of molecular sciences · 2026
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  18. The research progress in the interaction betweenFrontiers in microbiology · 2022
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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.

Pei YeNanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China.
Wei ChenNanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China.
Fan HuangNanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China.
Qin LiuNanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China.
Ya-Nan ZhuNanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China.
Xiang WangNanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China.
Xiao-Dong HanNanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China.
Wen-Mei WangNanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China.
Nanjing Medical University · CNNanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Smoking and Candida albicans (C. albicans) infection are risk factors for many oral diseases. Several studies have reported a close relationship between smoking and the occurrence of C. albicans infection. However, the exact underlying mechanism of this relationship remains unclear. We established a rat infection model and a C. albicans-Leuk1 epithelial cell co-culture model with and without smoke exposure to investigate the mechanism by which smoking contributes to C. albicans infection. Oral mucosa samples from healthy individuals and patients with oral leucoplakia were also analysed according to their smoking status. Our results indicated that smoking induced oxidative stress and redox dysfunction in the oral mucosa. Smoking-induced Nrf2 negatively regulated the NLRP3 inflammasome, impaired the oral mucosal defence response and increased the oral mucosa susceptibility to C. albicans. The results suggest that the Nrf2 pathway could be involved in the pathogenesis of oral diseases by mediating an antioxidative response to cigarette smoke exposure and suppressing host immunity against C. albicans.

Indexed as

AnimalsCandida albicansCandidiasisCell LineCigarette SmokingDisease Models, AnimalFemaleHumansInflammasomesIn Vitro TechniquesMaleMouth MucosaNF-E2-Related Factor 2RatsRats, WistarInflammasomesNF-E2-Related Factor 2Candida albicansNLRP3 inflammasomeNrf2oral immunityoxidative stresssmoking

Identifiers

PMID34155778
PMCPMC8358876
OpenAlexW3176535067

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.