ArticleScientific reports2016
Mycobacterium avium MAV2054 protein induces macrophage apoptosis by targeting mitochondria and reduces intracellular bacterial growth.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- The Cyclooxygenase 2 Inhibitor Etoricoxib as Adjunctive Therapy in Tuberculosis Impairs Macrophage Control of Mycobacterial Growth.The Journal of infectious diseases · 2024Trial
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- Encapsulin protein MAV2054 enhances Mycobacterium avium virulence by promoting Cdc42-dependent epithelial cell invasion.Journal of microbiology (Seoul, Korea) · 2025Article
- Cell death pathways in response toInfection and immunity · 2025Review
- Exploring the Chemical Space of Mycobacterial Oxidative Phosphorylation Inhibitors Using Molecular Modeling.ChemMedChem · 2024Review
- Effect and Mechanism of Mycobacterium avium MAV-5183 on Apoptosis of Mouse Ana-1 Macrophages.Cell biochemistry and biophysics · 2024Article
- The Role of Immune Dysfunction in Parkinson's Disease Development.International journal of molecular sciences · 2023Review
- Meeting the challenges of NTM-PD from the perspective of the organism and the disease process: innovations in drug development and delivery.Respiratory research · 2022Review
- Sputum Metabolites Associated with Nontuberculous Mycobacterial Infection in Cystic Fibrosis.mSphere · 2022Article
- Encapsulins.Annual review of biochemistry · 2022Review
- Modulating macrophage function to reinforce host innate resistance againstFrontiers in immunology · 2022Review
- The Role of NRF2 in Mycobacterial Infection.Antioxidants (Basel, Switzerland) · 2021Review
- Liposomal drug delivery to manage nontuberculous mycobacterial pulmonary disease and other chronic lung infections.European respiratory review : an official journal of the European Respiratory Society · 2021Review
- Genetic Involvement ofInternational journal of molecular sciences · 2021Review
- The role of mitophagy in innate immune responses triggered by mitochondrial stress.Cell communication and signaling : CCS · 2020Review
- Antigen-Specific IFN-γ/IL-17-Co-Producing CD4Vaccines · 2020Article
- Mycobacterial Control of Host Mitochondria: Bioenergetic and Metabolic Changes Shaping Cell Fate and Infection Outcome.Frontiers in cellular and infection microbiology · 2020Review
- Reactive oxygen species-mediated endoplasmic reticulum stress response induces apoptosis of Mycobacterium avium-infected macrophages by activating regulated IRE1-dependent decay pathway.Cellular microbiology · 2019Article
- The influence of PMExperimental and therapeutic medicine · 2019Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium avium complex induces macrophage apoptosis. However, the M. avium components that inhibit or trigger apoptosis and their regulating mechanisms remain unclear. We recently identified the immunodominant MAV2054 protein by fractionating M. avium culture filtrate protein by multistep chromatography; this protein showed strong immuno-reactivity in M. avium complex pulmonary disease and in patients with tuberculosis. Here, we investigated the biological effects of MAV2054 on murine macrophages. Recombinant MAV2054 induced caspase-dependent macrophage apoptosis. Enhanced reactive oxygen species production and JNK activation were essential for MAV2054-mediated apoptosis and MAV2054-induced interleukin-6, tumour necrosis factor, and monocyte chemoattractant protein-1 production. MAV2054 was targeted to the mitochondrial compartment of macrophages treated with MAV2054 and infected with M. avium. Dissipation of the mitochondrial transmembrane potential (ΔΨ
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Registered trials
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.