ArticleFrontiers in physiology2012
NF-κB Signaling Dynamics Play a Key Role in Infection Control in Tuberculosis.
Article in Frontiers in physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 105 citations in OpenAlex.
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- YY1 Contributes to the Inflammatory Responses of Mycobacterium tuberculosis-Infected Macrophages Through Transcription Activation-Mediated Upregulation TLR4.Molecular biotechnology · 2025Article
- Differential Host Gene Expression in Response to Infection by DifferentMicroorganisms · 2024Article
- Immunoinhibitory effects of anti-tuberculosis therapy induce the host vulnerability to tuberculosis recurrence.Microbiology spectrum · 2024Article
- Agent-based model predicts that layered structure and 3D movement work synergistically to reduce bacterial load in 3D in vitro models of tuberculosis granuloma.PLoS computational biology · 2024Article
- Mycobacterial Rv1804c binds to the PEST domain of IκBα and activates macrophage-mediated proinflammatory responses.iScience · 2024Article
- In silico agent-based modeling approach to characterize multiple in vitro tuberculosis infection models.PloS one · 2024Article
- Understanding the development of tuberculous granulomas: insights into host protection and pathogenesis, a review in humans and animals.Frontiers in immunology · 2024Review
- Role of NF-κB duringInternational journal of molecular sciences · 2023Review
- A framework for multi-scale intervention modeling: virtual cohorts, virtual clinical trials, and model-to-model comparisons.Frontiers in systems biology · 2023Article
- Article
- Systematic comparison of differential expression networks in MTB mono-, HIV mono- and MTB/HIV co-infections for drug repurposing.PLoS computational biology · 2022Article
- Integrating central nervous system metagenomics and host response for diagnosis of tuberculosis meningitis and its mimics.Nature communications · 2022Article
- Is the course of COVID-19 associated with tuberculin skin test diameter? A retrospective study.Journal of medical virology · 2022Article
- Anti-inflammatory and anti-oxidant properties of Melianodiol on DSS-induced ulcerative colitis in mice.PeerJ · 2022Article
- Intranasal immunization with peptide-based immunogenic complex enhances BCG vaccine efficacy in a murine model of tuberculosis.JCI insight · 2021Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The NF-κB signaling pathway is central to the body's response to many pathogens. Mathematical models based on cell culture experiments have identified important molecular mechanisms controlling the dynamics of NF-κB signaling, but the dynamics of this pathway have never been studied in the context of an infection in a host. Here, we incorporate these dynamics into a virtual infection setting. We build a multi-scale model of the immune response to the pathogen Mycobacterium tuberculosis (Mtb) to explore the impact of NF-κB dynamics occurring across molecular, cellular, and tissue scales in the lung. NF-κB signaling is triggered via tumor necrosis factor-α (TNF) binding to receptors on macrophages; TNF has been shown to play a key role in infection dynamics in humans and multiple animal systems. Using our multi-scale model, we predict the impact of TNF-induced NF-κB-mediated responses on the outcome of infection at the level of a granuloma, an aggregate of immune cells and bacteria that forms in response to infection and is key to containment of infection and clinical latency. We show how the stability of mRNA transcripts corresponding to NF-κB-mediated responses significantly controls bacterial load in a granuloma, inflammation level in tissue, and granuloma size. Because we incorporate intracellular signaling pathways explicitly, our analysis also elucidates NF-κB-associated signaling molecules and processes that may be new targets for infection control.
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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.