Evidence map›Paper›PMID 39639253›Full record

ArticleBMC oral health2024

Porphyromonas gingivalis inducing autophagy-related biological dysfunction in alveolar epithelial cells: an in vitro study.

Qian Zhao, Xueyuan Wang, Wenyan Liu, Huan Tian, Hongjia Yang, Zuomin Wang, Zhiqiang Liu

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PubMed Full text at PMC Publisher
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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–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

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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

3 citing papers in PubMed.

  1. Review
  2. Synergistic effects ofFrontiers in cellular and infection microbiology · 2025
    Article
  3. 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

7 authors.

Qian Zhao *Department of Stomatology, Beijing Chao-Yang Hospital, Capital Medical University, 8 Gongti South Road, Chaoyang District, Beijing, 100020, China.
Xueyuan Wang *Department of Stomatology, Beijing Chao-Yang Hospital, Capital Medical University, 8 Gongti South Road, Chaoyang District, Beijing, 100020, China.
Wenyan LiuDepartment of Stomatology, Beijing Lu He Hospital, Capital Medical University, Beijing, China.
Huan TianDepartment of Special Clinic Center, Changsha Stomatological Hospital, Hunan University of Traditional Chinese Medicine, Changsha, China.
Hongjia YangDepartment of Stomatology, Beijing Chao-Yang Hospital, Capital Medical University, 8 Gongti South Road, Chaoyang District, Beijing, 100020, China.
Zuomin WangDepartment of Stomatology, Beijing Chao-Yang Hospital, Capital Medical University, 8 Gongti South Road, Chaoyang District, Beijing, 100020, China. wzuomin@sina.cn.
Zhiqiang LiuDepartment of Stomatology, Beijing Chao-Yang Hospital, Capital Medical University, 8 Gongti South Road, Chaoyang District, Beijing, 100020, China. kokorora@sina.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic obstructive pulmonary disease (COPD) is a respiratory disease with high morbidity and mortality. Notably, the pathogenesis and progression of COPD are related to lung infection, inflammatory response, and biological dysfunction in alveolar epithelial cells. Studies also found that periodontitis is an independent risk factor for COPD. The inhalation of periodontal pathogens into the respiratory system is the most common method for periodontal pathogens to promote the development of COPD. Porphyromonas gingivalis (P. gingivalis), the keystone pathogen in periodontitis, has been found to migrate to the lungs, triggering inflammatory reactions and causing decreased lung function. However, the impact of P. gingivalis infection on the biological function of alveolar epithelial cells remains unclear. Therefore, this study aimed to investigate the effects of P. gingivalis infection on the biological functions of alveolar epithelial cells.

methodsMouse alveolar epithelial cells (MLE-12) were co-cultured with P. gingivalis and treated with autophagy inhibitor chloroquine (CQ) or LC3 siRNA in vitro. MTT assay and EdU staining were used to detect cell viability, and the TUNEL assay kit and Annexin V-FITC/PI method were used to detect cell apoptosis. Western blot was used to detect autophagic markers LC3 and P62, and mRFP-GFP-LC3 was used to observe autophagic flux.

resultsP. gingivalis inhibited the viability of alveolar epithelial cells in a dose- and time-dependent manner. P. gingivalis also promoted autophagy and apoptosis of alveolar epithelial cells in a dose-dependent manner. Interestingly, we found that inhibiting autophagy using CQ or silencing LC3 with siRNA significantly reduced cell apoptosis and viability damage induced by P. gingivalis. Thus, these data indicated the synergistic effect of autophagy in P. gingivalis-induced biological dysfunction of alveolar epithelial cells.

conclusionP. gingivalis infection can cause biological dysfunction of alveolar epithelial cells, manifested as decreased cell viability, increased autophagy and apoptosis. Notably, the up-regulation of autophagy induced by P. gingivalis plays a synergistic role in this dysfunction.

Indexed as

ApoptosisAutophagyPorphyromonas gingivalisAlveolar Epithelial CellsAnimalsCell LineCell SurvivalChloroquineEpithelial CellsIn Vitro TechniquesMiceMicrotubule-Associated ProteinsRNA, Small InterferingChloroquineMicrotubule-Associated ProteinsRNA, Small InterferingAlveolar epithelial cellApoptosisAutophagyPorphyromonas gingivalis

Identifiers

PMID39639253
PMCPMC11619664

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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.