Evidence map›Paper›PMID 39702141›Full record

ArticleBMC oral health2024

Guanylate-binding protein 5-mediated autophagy can promote the clearance of intracellular F. nucleatum in dental pulp cells during pulpitis.

Minchun Huang, Bo Yang, Xiaojun Yang, Jin Hou, Xinzhu Li

Abstract read
In one paragraph

Article in BMC oral health, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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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

5 authors.

Minchun HuangDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Bo YangDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Xiaojun YangDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Jin HouDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. houjin@smu.edu.cn.
Xinzhu LiDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. lixinzhu880623@i.smu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIFN-γ is crucial in induction of inducible cell-autonomous immunity, and IFN-γ signaling pathway is activated in pulpitis. Guanylate-binding proteins (GBPs) are a family of IFN-inducible GTPases and could utilize autophagy or pyroptosis to mitigate infection. GBP5 is abundantly expressed in inflamed pulp and human dental pulp cells (HDPCs). Therefore, we hypothesize that GBP5 in HDPCs exerts an immune-regulatory role in defending against bacterium infection.

methodsFusobacterium nucleatum (F. nucleatum) was used to infect HDPCs, and immunoblotting and qRT-PCR were used to detect pyroptosis and autophagy. Pharmacological or genetic approaches were used to enhance or knock down GBP5 expression in HDPCs. Blood agar plate counting and immunoblotting were used to observe bacteria clearance effect and activation of autophagy. Student's t-test and one-way ANOVA were individually used for comparisons between two and multiple groups. Statistical significance was set at P < 0.05.

resultsFollowing F. nucleatum infection in HDPCs, the autophagy marker LC3B was significantly upregulated while the mRNA and protein expression levels of p62 were increased. IFN-γ priming significantly inhibited the intracellular survival of F. nucleatum and enhanced the autophagic activity of HDPCs. GBP5 overexpression significantly increased the efficiency of HDPCs in clearing intracellular F. nucleatum and activated autophagic flux in HDPCs, while downregulating GBP5 in HDPCs suppressed autophagic flux.

conclusionIFN-γ-mediated GBP5 overexpression in HDPCs during F. nucleatum infection exerts an anti-microbial function through autophagy activation.

Indexed as

AutophagyDental PulpFusobacterium nucleatumGTP-Binding ProteinsPulpitisCells, CulturedHumansInterferon-gammaGTP-Binding ProteinsInterferon-gammaAutophagyGuanylate-binding protein 5Human dental pulp cellsInterferon-γ (IFN-γ)Pulpitis

Identifiers

PMID39702141
PMCPMC11660433

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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.