ArticlePloS one2013
Pre-exposure of Mycobacterium tuberculosis-infected macrophages to crystalline silica impairs control of bacterial growth by deregulating the balance between apoptosis and necrosis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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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
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- The association between silica exposure, silicosis and tuberculosis: a systematic review and meta-analysis.BMC public health · 2021Pooled it
- Cutting for Stone: A Case Report of Isolated Pleural Silicosis in an Engineered Stone Fabrication Worker.CHEST pulmonary · 2025Article
- A review of silicosis and other silica-related diseases in the engineered stone countertop processing industry.Journal of occupational medicine and toxicology (London, England) · 2025Review
- Silicotuberculosis: a critical narrative review.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Toxicity and Impact of Silica Nanoparticles on the Configuration of Gut Microbiota in Immunodeficient Mice.Microorganisms · 2023Article
- Diverse Cell Death Mechanisms Are Simultaneously Activated in Macrophages Infected by VirulentPathogens (Basel, Switzerland) · 2022Article
- Immunity to the Dual Threat of Silica Exposure andFrontiers in immunology · 2018Review
- Macrophage Exposure to Polycyclic Aromatic Hydrocarbons From Wood Smoke Reduces the Ability to Control Growth ofFrontiers in medicine · 2018Article
- Acute Exposure to Crystalline Silica Reduces Macrophage Activation in Response to Bacterial Lipoproteins.Frontiers in immunology · 2016Article
- Low Dose BCG Infection as a Model for Macrophage Activation Maintaining Cell Viability.Journal of immunology research · 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
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhalation of crystalline silica (CS) particles increases the risk of pulmonary tuberculosis; however, the precise mechanism through which CS exposure facilitates Mycobacterium tuberculosis (Mtb) infection is unclear. We speculate that macrophage exposure to CS deregulates the cell death pathways that could explain, at least in part, the association observed between exposure to CS and pulmonary tuberculosis. We therefore established an in vitro model in which macrophages were exposed to CS and then infected with Mtb. Expression of surface markers was analyzed by flow cytometry, JNK1/2, ASK1, caspase 9, P-p38, Bcl-2 and Mcl-1 were analyzed by Western blot, and cytokines by ELISA. Our results show that exposure to CS limits macrophage ability to control Mtb growth. Moreover, this exposure reduced the expression of TLR2, Bcl-2 and Mcl-1, but increased that of JNK1 and ASK1 molecules in the macrophages. Finally, when the pre-exposed macrophages were infected with Mtb, the concentrations of TNFα, IL-1β and caspase-9 expression increased. This pro-inflammatory profile of the macrophage unbalanced the apoptosis/necrosis pathway. Taken together, these data suggest that macrophages exposed to CS are sensitized to cell death by MAPK kinase-dependent signaling pathway. Secretion of TNF-α and IL-1β by Mtb-infected macrophages promotes necrosis, and this deregulation of cell death pathways may favor the release of viable bacilli, thus leading to the progression of tuberculosis.
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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.