Evidence map›Paper›PMID 29500439›Full record

ArticleCell death & disease2018

Indoleamine 2,3-dioxygenase expression regulates the survival and proliferation of Fusobacterium nucleatum in THP-1-derived macrophages.

Ying Xue, Han Xiao, Songhe Guo, Banglao Xu, Yuehua Liao, Yixian Wu, Ge Zhang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
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  18. The oral-gut microbiome axis in health and disease.Nature reviews. Microbiology · 2024
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Ying XueSchool of Public Health (Shenzhen), Sun Yat-sen University, Guangdong, China.
Han XiaoDepartment of Microbial and Biochemical Pharmacy, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.
Songhe GuoDepartment of Microbial and Biochemical Pharmacy, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.
Banglao XuDepartment of Clinical Laboratory Medicine, Guangzhou First Municipal People's Hospital, Guangzhou Medical University, Guangzhou, China.
Yuehua LiaoDepartment of Microbial and Biochemical Pharmacy, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.
Yixian WuDepartment of Microbial and Biochemical Pharmacy, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.
Ge ZhangSchool of Public Health (Shenzhen), Sun Yat-sen University, Guangdong, China. zhangge@mail.sysu.edu.cn.
Sun Yat-sen University · CNGuangzhou First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fusobacterium nucleatum (Fn) is a tumor-associated obligate anaerobic bacterium, which has a role in the progression of colorectal cancer (CRC). Fn can invade and promote colon epithelial cells proliferation. However, how Fn survives and proliferates in its host cells remains largely unknown. In this study, we aimed to determine the molecular mechanisms underlying the morphology, survival, and proliferation of Fn in THP-1-derived macrophages (dTHP1). For the first time, we found that Fn is a facultative intracellular bacterium that can survive and limited proliferate in dTHP1 cells up to 72 h, and a live Fn infection can inhibit apoptosis of dTHP1 cells by activating the PI3K and ERK pathways. Both Fn bacteria and dTHP1 cells exhibit obvious morphological changes during infection. In addition, Infection of Fn-induced indoleamine 2,3-dioxygenase (IDO) expression by TNF-α-dependent and LPS-dependent pathway in a time-dependent and dose-dependent manner, and the IDO-induced low tryptophan and high kynurenine environment inhibited the intracellular multiplication of Fn in dTHP1 cells. IDO expression further impaired the function of peripheral blood lymphocytes, permitting the escape of Fn-infected macrophages from cell death. IDO inhibition abrogated this effect caused by Fn and relieved immune suppression. In conclusion, we identified IDO as an important player mediating intracellular Fn proliferation in macrophages, and inhibition of IDO may aggravate infection in Fn-associated tumor immunotherapy.

Indexed as

ApoptosisCell ProliferationCell SurvivalFusobacterium InfectionsFusobacterium nucleatumHumansIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-gammaInterleukin-6KynurenineLymphocytesMacrophagesMAP Kinase Signaling SystemPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTHP-1 CellsIDO1 protein, humanIL6 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-gammaInterleukin-6KynureninePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTryptophanTumor Necrosis Factor-alpha

Identifiers

PMID29500439
PMCPMC5834448
OpenAlexW2793337761

What OpenQuestion holds

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Registered trials

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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.