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Identification of Host-Targeted Small Molecules That Restrict Intracellular Mycobacterium tuberculosis Growth
Open accessAbstract
Mycobacterium tuberculosis remains a significant threat to global health. Macrophages are the host cell for M. tuberculosis infection, and although bacteria are able to replicate intracellularly under certain conditions, it is also clear that macrophages are capable of killing M. tuberculosis if appropriately activated. The outcome of infection is determined at least in part by the host-pathogen interaction within the macrophage; however, we lack a complete understanding of which host pathways are critical for bacterial survival and replication. To add to our understanding of the molecular processes involved in intracellular infection, we performed a chemical screen using a high-content microscopic assay to identify small molecules that restrict mycobacterial growth in macrophages by targeting host functions and pathways. The identified host-targeted inhibitors restrict bacterial growth exclusively in the context of macrophage infection and predominantly fall into five categories: G-protein coupled receptor modulators, ion channel inhibitors, membrane transport proteins, anti-inflammatories, and kinase modulators. We found that fluoxetine, a selective serotonin reuptake inhibitor, enhances secretion of pro-inflammatory cytokine TNF-α and induces autophagy in infected macrophages, and gefitinib, an inhibitor of the Epidermal Growth Factor Receptor (EGFR), also activates autophagy and restricts growth. We demonstrate that during infection signaling through EGFR activates a p38 MAPK signaling pathway that prevents macrophages from effectively responding to infection. Inhibition of this pathway using gefitinib during in vivo infection reduces growth of M. tuberculosis in the lungs of infected mice. Our results support the concept that screening for inhibitors using intracellular models results in the identification of tool compounds for probing pathways during in vivo infection and may also result in the identification of new anti-tuberculosis agents that work by modulating host pathways. Given the existing experience with some of our identified compounds for other therapeutic indications, further clinically-directed study of these compounds is merited.
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“Specifically, fluoxetine, a selective serotoine re-uptake inhibitor, and gefitinib, an inhibitor of epidermal growth factor receptor (EGFR) activity stimulated autophagy and reduced intra-macrophage survival of M. tuberculosis.”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [80]
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“The effect of gefitinib could be traced back to blockade of EGFR mediated p38-MAPK activation, a known inhibitory pathway of autophagy (80).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [80]
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Metadata
- Authors
- Stanley, S. A., Barczak, A. K., Silvis, M. R., Luo, S. S., Sogi, K., Vokes, M., Bray, M.-A., Carpenter, A. E., Moore, C. B., Siddiqi, N., Rubin, E. J., & Hung, D. T.
- Affiliations
- Broad Institute (US)
- University of California, Berkeley (US)
- Harvard University (US)
- Corresponding author
- Hung, Deborah T.
- ORCID
- Venue
- PLoS Pathogens
- Publisher
- Public Library of Science (PLoS)
- Published
- 2014-02-20
- Volume
- 10
- Issue
- 2
- Pages
- e1003946
- ISSN
- 1553-7366 (ISSN-L)
- 1553-7374
- PMC
- PMC3930586
- OpenAlex
- W2009324985
- Cited by
- 251
- References
- 63
- Citations by year
- 2026: 15 · 2025: 10 · 2024: 14 · 2023: 8 · 2022: 19 · 2021: 35 · 2020: 24 · 2019: 18 · 2018: 19 · 2017: 21 · 2016: 32 · 2015: 30 · 2014: 6
- FWCI
- 20.78
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS Pathogens (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- Helen Hay Whitney Foundation
- Broad Institute
- National Institutes of Health (NIH-R01)
- National Institute of General Medical Sciences (R01GM089652)
- National Institute of Allergy and Infectious Diseases (K08AI080944, T32AI007061)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
- Health Sciences › Medicine › Infectious Diseases › Infectious Diseases and Tuberculosis
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Keywords
- Mycobacterium tuberculosis, host-pathogen interaction, macrophages, intracellular bacterial growth, autophagy, TNF-alpha secretion, gefitinib, EGFR signaling, p38 MAPK signaling, fluoxetine, tuberculosis drug discovery, ion channel inhibitors
- MeSH terms
- Animals, Antitubercular Agents, Disease Models, Animal, Macrophages, Male, Mice, Inbred BALB C, Mice, Inbred C57BL, Mycobacterium tuberculosis, Tuberculosis, Signal Transduction, Mice, Host-Pathogen Interactions, High-Throughput Screening Assays
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