ArticleACS infectious diseases2017
The Tyrosine Kinase Inhibitor Gefitinib Restricts Mycobacterium tuberculosis Growth through Increased Lysosomal Biogenesis and Modulation of Cytokine Signaling.
Article in ACS infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- Host-directed therapeutics against antimicrobial-resistant bacterial infections: emerging roles of multi-omics and systems biology.Frontiers in pharmacology · 2026Review
- Systems-level characterization of EGFR kinase inhibitors reveals heterogeneous effects on Mtb-macrophage interactions.bioRxiv : the preprint server for biology · 2025Article
- Host-directed therapeutic targets in macrophages and their ligands against mycobacteria tuberculosis.Infection and immunity · 2025Review
- Scaffold Hopping Strategy toward New 4‑Aminoquinazolines Active Against Extracellular and Intracellular.ACS medicinal chemistry letters · 2025Article
- Host-directed therapy for tuberculosis.European journal of medical research · 2025Review
- Decellularization of various tissues and organs through chemical methods.Tissue & cell · 2024Review
- Identification of kinase inhibitors as potential host-directed therapies for intracellular bacteria.Scientific reports · 2024Article
- Mycobacterium tuberculosis resides in lysosome-poor monocyte-derived lung cells during chronic infection.PLoS pathogens · 2024Article
- Review
- Deficiency in Galectin-3, -8, and -9 impairs immunity to chronic Mycobacterium tuberculosis infection but not acute infection with multiple intracellular pathogens.PLoS pathogens · 2023Article
- Potential Repurposed Drug Candidates for Tuberculosis Treatment: Progress and Update of Drugs Identified in Over a Decade.ACS omega · 2023Review
- Autophagy restricts Mycobacterium tuberculosis during acute infection in mice.Nature microbiology · 2023Article
- Host-directed therapy against tuberculosis: Concept and recent developments.Journal of biosciences · 2023Review
- Interactions of Autophagy and the Immune System in Health and Diseases.Autophagy reports · 2022Article
- Progressive Host-Directed Strategies to Potentiate BCG Vaccination Against Tuberculosis.Frontiers in immunology · 2022Review
- Recent Advances in Host-Directed Therapies for Tuberculosis and Malaria.Frontiers in cellular and infection microbiology · 2022Review
- Host-directed therapy to combat mycobacterial infections.Immunological reviews · 2021Review
- The Prospect of Repurposing Immunomodulatory Drugs for Adjunctive Chemotherapy against Tuberculosis: A Critical Review.Antibiotics (Basel, Switzerland) · 2021Review
- Immune Subtyping in Latent Tuberculosis.Frontiers in immunology · 2021Article
- Gefitinib Results in Robust Host-Directed Immunity AgainstFrontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Host-directed therapeutics have the potential to combat the global tuberculosis pandemic. We previously identified gefitinib, an inhibitor of EGFR, as a potential host-targeted therapeutic effective against Mycobacterium tuberculosis infection of macrophages and mice. Here we examine the functional consequences of gefitinib treatment on M. tuberculosis infected macrophages. Using phosphoproteomic and transcriptional profiling, we identify two mechanisms by which gefitinib influences macrophage responses to infection to affect cytokine responses and limit replication of M. tuberculosis in macrophages. First, we find that gefitinib treatment of M. tuberculosis infected macrophages inhibits STAT3, a transcription factor known to repress effective immune responses to M. tuberculosis in vivo. Second, we find that gefitinib treatment of M. tuberculosis infected macrophages leads to increased expression of genes involved in lysosomal biogenesis and function and an increase of functional lysosomes in gefitinib treated cells. Furthermore, we show that gefitinib treatment increases the targeting of bacteria to lysosomes, providing an explanation for the cell intrinsic effects of gefitinib treatment on M. tuberculosis infection. Our data provide novel insights into the effects of gefitinib on mammalian cells and into the possible roles for EGFR signaling in macrophages.
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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.