Evidence map›Paper›PMID 39819414›Full record

ArticleCurrent molecular medicine2025

Ag85B-induced M1 Macrophage Polarization via the TLR4/TRAF6/NF-κB Axis Leading to Bronchial Epithelial Cell Damage and TH17/Treg Imbalance.

Lei Zhou, Li Luo, Linzi Luo, Hailong Luo, Yan Ding, Zhibin Lu, Yangbao Xiao

Abstract read
PubMed Publisher
In one paragraph

Article in Current molecular medicine, 2025. 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

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

1 citing paper in PubMed.

  1. 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.

Lei ZhouEndoscopy Center, Hunan Chest Hospital, Hunan Provincial Center for Disease Control and Prevention, Changsha, 410016, China.
Li LuoEndoscopy Center, Hunan Chest Hospital, Hunan Provincial Center for Disease Control and Prevention, Changsha, 410016, China.
Linzi LuoEndoscopy Center, Hunan Chest Hospital, Hunan Provincial Center for Disease Control and Prevention, Changsha, 410016, China.
Hailong LuoEndoscopy Center, Hunan Chest Hospital, Hunan Provincial Center for Disease Control and Prevention, Changsha, 410016, China.
Yan DingEndoscopy Center, Hunan Chest Hospital, Hunan Provincial Center for Disease Control and Prevention, Changsha, 410016, China.
Zhibin LuEndoscopy Center, Hunan Chest Hospital, Hunan Provincial Center for Disease Control and Prevention, Changsha, 410016, China.
Yangbao XiaoEndoscopy Center, Hunan Chest Hospital, Hunan Provincial Center for Disease Control and Prevention, Changsha, 410016, China.

Funding

Clinical Medical Technology Innovation Guidance Project of Hunan Province 2021SK50701Hunan Chest Hospital 2022 annual hospital project SXK2022009National Key Clinical Specialty Scientific Research Project Z2023075
6 · The paper itself

Abstract

backgroundAntigen 85B (Ag85B) is a signature antigen of Mycobacterium tuberculosis (MTB). In this study, we aimed to investigate the impact of macrophages stimulated with Ag85B on bronchial epithelial cells and T cells, as well as the underlying mechanisms involved.

methodsWe used Ag85B to stimulate macrophage and investigated the impact of Ag85B on macrophage polarization. We assessed the impact of TLR4 on Ag85Bmediated macrophage polarization by silencing TLR4. Additionally, the regulatory role of TLR4 on the TRAF6/NF-κB pathway was evaluated through immunoblotting. Activated macrophages with Ag85B were co-cultured with mouse bronchial epithelial cells (MBECs) and T cells, respectively. Through immunoblotting quantification, biochemical methods, and flow cytometry, we explored the effects and molecular mechanisms of Ag85B-induced macrophage activation on bronchial epithelial cell damage and T-cell transformation.

resultsIn macrophages stimulated with Ag85B, levels of M1 polarization-related genes (CXCL9, CXCL10, and iNOS) and cytokines (IL-6, TNF-α, IL-1β, and IL-12) were increased, and the M1/M2 ratio was elevated. TLR4 silence inhibited the effects of Ag85B on macrophages and decreased TRAF6 and p-NF-κB/NF-κB levels. TRAF6 overexpression reversed the inhibitory effect of TLR4 on macrophage stimulation with Ag85B. After co-culturing with macrophages induced by Ag85B, MBEC cell proliferation was inhibited, apoptosis was promoted, and the TH17/Treg ratio of T cells was increased. Silencing TLR4 reversed the impact of Ag85B-induced macrophage polarization on bronchial epithelial cells and T cells, which was further reversed by TRAF6 overexpression.

conclusionAg85B promoted M1 polarization in macrophages through the TLR4/TRAF6/NF-κB axis, resulting in bronchial epithelial cell damage and an imbalance in TH17/Treg cells.

Indexed as

AcyltransferasesAntigens, BacterialBronchiEpithelial CellsMacrophagesNF-kappa BTh17 CellsTNF Receptor-Associated Factor 6Toll-Like Receptor 4AnimalsCell PolarityHumansMacrophage ActivationMiceMycobacterium tuberculosisSignal TransductionAcyltransferasesAntigens, BacterialNF-kappa BTlr4 protein, mouseTNF Receptor-Associated Factor 6Toll-Like Receptor 4TRAF6 protein, mouseAg85Bbronchial epithelial cellsmacrophagesMycobacterium tuberculosis.TH17/TregTLR4/TRAF6/NF-κB

Identifiers

PMID39819414

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.