ArticlePLoS pathogens2011
Targeting of Mycobacterium tuberculosis heparin-binding hemagglutinin to mitochondria in macrophages.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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.
Who cites it
30 citing papers in PubMed, 63 citations in OpenAlex.
- Structural and Functional Characterization of Protein Adhesins and Pili in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Article
- Effect and Mechanism of Mycobacterium avium MAV-5183 on Apoptosis of Mouse Ana-1 Macrophages.Cell biochemistry and biophysics · 2024Article
- Role of C-terminal domain of Mycobacterium tuberculosis PE6 (Rv0335c) protein in host mitochondrial stress and macrophage apoptosis.Apoptosis : an international journal on programmed cell death · 2023Article
- Mycobacterial Adhesion: From Hydrophobic to Receptor-Ligand Interactions.Microorganisms · 2022Review
- Article
- Type I interferon decreases macrophage energy metabolism during mycobacterial infection.Cell reports · 2021Article
- Reduction of host cell mitochondrial activity as Mycobacterium leprae's strategy to evade host innate immunity.Immunological reviews · 2021Review
- Mitochondria: Powering the Innate Immune Response to Mycobacterium tuberculosis Infection.Infection and immunity · 2021Review
- Mycobacterium tuberculosis infection up-regulates MFN2 expression to promote NLRP3 inflammasome formation.The Journal of biological chemistry · 2020Article
- The role of mitophagy in innate immune responses triggered by mitochondrial stress.Cell communication and signaling : CCS · 2020Review
- NAD hydrolysis by the tuberculosis necrotizing toxin induces lethal oxidative stress in macrophages.Cellular microbiology · 2020Article
- Host Cell Targets of Released Lipid and Secreted Protein Effectors ofFrontiers in cellular and infection microbiology · 2020Review
- Mycobacterial Control of Host Mitochondria: Bioenergetic and Metabolic Changes Shaping Cell Fate and Infection Outcome.Frontiers in cellular and infection microbiology · 2020Review
- L-Cystathionine Protects against Homocysteine-Induced Mitochondria-Dependent Apoptosis of Vascular Endothelial Cells.Oxidative medicine and cellular longevity · 2019Article
- NADCell reports · 2018Article
- Phagocytosis influences the intracellular survival ofCell & bioscience · 2018Article
- Mycobacterium abscessus glycopeptidolipids inhibit macrophage apoptosis and bacterial spreading by targeting mitochondrial cyclophilin D.Cell death & disease · 2017Article
- Role of apoptosis and autophagy in tuberculosis.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- Inhibition of apoptosis by Rv2456c through Nuclear factor-κB extends the survival of Mycobacterium tuberculosis.International journal of mycobacteriology · 2016Article
- Mycobacterium avium MAV2054 protein induces macrophage apoptosis by targeting mitochondria and reduces intracellular bacterial growth.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium tuberculosis heparin-binding hemagglutinin (HBHA), a virulence factor involved in extrapulmonary dissemination and a strong diagnostic antigen against tuberculosis, is both surface-associated and secreted. The role of HBHA in macrophages during M. tuberculosis infection, however, is less well known. Here, we show that recombinant HBHA produced by Mycobacterium smegmatis effectively induces apoptosis in murine macrophages. DNA fragmentation, nuclear condensation, caspase activation, and poly (ADP-ribose) polymerase cleavage were observed in apoptotic macrophages treated with HBHA. Enhanced reactive oxygen species (ROS) production and Bax activation were essential for HBHA-induced apoptosis, as evidenced by a restoration of the viability of macrophages pretreated with N-acetylcysteine, a potent ROS scavenger, or transfected with Bax siRNA. HBHA is targeted to the mitochondrial compartment of HBHA-treated and M. tuberculosis-infected macrophages. Dissipation of the mitochondrial transmembrane potential (ΔΨ(m)) and depletion of cytochrome c also occurred in both macrophages and isolated mitochondria treated with HBHA. Disruption of HBHA gene led to the restoration of ΔΨ(m) impairment in infected macrophages, resulting in reduced apoptosis. Taken together, our data suggest that HBHA may act as a strong pathogenic factor to cause apoptosis of professional phagocytes infected with M. tuberculosis.
Indexed as
Identifiers
What OpenQuestion holds
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.