ArticlePloS one2016
The Defect in Autophagy Induction by Clinical Isolates of Mycobacterium Tuberculosis Is Correlated with Poor Tuberculosis Outcomes.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Furamidine enhances IL-23-mediated autophagic response through IL-23R-TYK2-STAT3-dependent regulation of intracellular Ca²⁺ level to facilitate mycobacterial clearance in human macrophages.Medical microbiology and immunology · 2025Article
- rBCG-LTAK63 enhances protection against tuberculosis by inducing autophagy and circadian gene regulation.Frontiers in immunology · 2025Article
- Beyond the Clinic: The Activation of Diverse Cellular and Humoral Factors Shapes the Immunological Status of Patients with Active Tuberculosis.International journal of molecular sciences · 2023Review
- Measurement of Autophagy Activity Reveals Time-Dependent, Bacteria-Specific Turnover duringPathogens (Basel, Switzerland) · 2022Article
- Mycobacterium tuberculosis Rv0790c inhibits the cellular autophagy at its early stage and facilitates mycobacterial survival.Frontiers in cellular and infection microbiology · 2022Article
- It Takes a Village: The Multifaceted Immune Response toFrontiers in immunology · 2022Review
- Shedding Light on Autophagy During Human Tuberculosis. A Long Way to Go.Frontiers in cellular and infection microbiology · 2021Review
- Targeting Autophagy as a Strategy for Developing New Vaccines and Host-Directed Therapeutics Against Mycobacteria.Frontiers in microbiology · 2020Review
- The Immune Mechanisms of Lung Parenchymal Damage in Tuberculosis and the Role of Host-Directed Therapy.Frontiers in microbiology · 2018Review
- Role of apoptosis and autophagy in tuberculosis.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- Integrating Lung Physiology, Immunology, and Tuberculosis.Trends in microbiology · 2017Review
- [Visualized detection for mycobacterium tuberculosis using loop-mediated isothermal amplification assay].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2017Article
- Autophagy Is an Innate Mechanism Associated with Leprosy Polarization.PLoS pathogens · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTuberculosis (TB) represents a major global health problem. The prognosis of clinically active tuberculosis depends on the complex interactions between Mycobacterium tuberculosis (Mtb) and its host. In recent years, autophagy receives particular attention for its role in host defense against intracellular pathogens, including Mtb. In present study, we aim to investigate the relationship of autophagy induction by clinical isolates of Mtb with the clinical outcomes in patients with TB. METHODOLOGY/PRINCIPAL
findingsWe collected 185 clinical isolates of Mtb, and determined the effect of these Mtb isolates on autophagy induction in macrophages. It was found that most of clinical isolates of Mtb were able to induce autophagosome formation in macrophages, however, the autophagy-inducing ability varied significantly among different isolates. Of importance, our results revealed that patients infected by Mtb with poor autophagy-inducing ability displayed more severe radiographic extent of disease (p<0.001), and were more likely to have unfavorable treatment outcomes (p<0.001). No significant association was observed between the extent of Mtb-induced autophagy with some socio-demographic characteristics (such as gender, age and tobacco consumption), and some laboratory tests (such as hemoglobin, leukocyte count and erythrocyte sedimentation rate). Furthermore, results from logistic regression analysis demonstrated that the defect in autophagy induction by clinical isolates of Mtb was an independent risk factor for far-advanced radiographic disease (aOR 4.710 [1.93-11.50]) and unfavorable treatment outcomes (aOR 8.309 [2.22-28.97]) in TB. CONCLUSION/SIGNIFICANCE: These data indicated that the defect in autophagy induction by Mtb isolates increased the risk of poor clinical outcomes in TB patients, and detection of clinical isolates-induced autophagosome formation might help evaluate the TB outcomes.
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