ArticleVirulence2016
Mycobacterium tuberculosis PPE68 and Rv2626c genes contribute to the host cell necrosis and bacterial escape from macrophages.
Article in Virulence, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Macrophage states and polarization duringFrontiers in cellular and infection microbiology · 2026Review
- Circulating antibody signatures againstFrontiers in immunology · 2026Article
- In silico framework for designing and validating a multi-stage subunit vaccine against Tuberculosis using reverse vaccinology approach.PloS one · 2026Article
- New and revised gene ontology biological process terms describe multiorganism interactions critical for understanding microbial pathogenesis and sequences of concern.Journal of biomedical semantics · 2025Article
- Single-cell analysis revealsScience advances · 2025Article
- The PE/PPE family proteins ofFrontiers in immunology · 2025Review
- Article
- Virulence Factors ofPathogens (Basel, Switzerland) · 2023Review
- Multi-omics-based characterization of the influences of Mycobacterium tuberculosis virulence factors EsxB and PPE68 on host cells.Archives of microbiology · 2023Article
- Immunological effects of the PE/PPE family proteins ofFrontiers in immunology · 2023Review
- The ESX-1 Substrate PPE68 Has a Key Function in ESX-1-Mediated Secretion in Mycobacterium marinum.mBio · 2022Article
- Article
- Different modalities of host cell death and their impact onAmerican journal of physiology. Cell physiology · 2022Review
- Two chronically misdiagnosed patients infected withFrontiers in cellular and infection microbiology · 2022Article
- Article
- Mycobacterium tuberculosis Rv2626c-derived peptide as a therapeutic agent for sepsis.EMBO molecular medicine · 2020Article
- The role of mitophagy in innate immune responses triggered by mitochondrial stress.Cell communication and signaling : CCS · 2020Review
- A multiple T cell epitope comprising DNA vaccine boosts the protective efficacy of Bacillus Calmette-Guérin (BCG) against Mycobacterium tuberculosis.BMC infectious diseases · 2020Article
- Competitive Cell Death Interactions in Pulmonary Infection: Host Modulation Versus Pathogen Manipulation.Frontiers in immunology · 2020Review
- IL-36γ Promotes Killing ofJournal of immunology (Baltimore, Md. : 1950) · 2019Article
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3 authors at 2 institutions in 1 country.
Funding
Abstract
Alveolar macrophages are the main line of innate immune response against M. tuberculosis (Mtb) infection. However, these cells serve as the major intracellular niche for Mtb enhancing its survival, replication and, later on, cell-to-cell spread. Mtb-associated cytotoxicity of macrophages has been well documented, but limited information exists about mechanisms by which the pathogen induces cell necrosis. To identify virulence factors involved in the induction of necrosis, we screened 5,000 transposon mutants of Mtb for clones that failed to promote the host cell necrosis in a similar manner as the wild-type bacterium. Five Mtb mutants were identified as potential candidates inducing significantly lower levels of THP-1 cell damage in contrast to the H37Rv wild-type infection. Reduced levels of the cell damage by necrosis deficient mutants (NDMs) were also associated with delayed damage of mitochondrial membrane permeability when compared with the wild-type infection over time. Two knockout mutants of the Rv3873 gene, encoding a cell wall PPE68 protein of RD1 region, were identified out of 5 NDMs. Further investigation lead to the observation that PPE68 protein interacts and exports several unknown or known surface/secreted proteins, among them Rv2626c is associated with the host cell necrosis. When the Rv2626c gene is deleted from the genome of Mtb, the bacterium displays significantly less necrosis in THP-1 cells and, conversely, the overexpression of Rv2626c promotes the host cell necrosis at early time points of infections in contrast to the wild-type strain.
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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.