ArticleJournal of inflammation (London, England)2016
Mycobacterium leprae alters classical activation of human monocytes in vitro.
Article in Journal of inflammation (London, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- AMetabolites · 2026Article
- Host-pathogen-immune interactions in an air-liquid interface airway model.Frontiers in cellular and infection microbiology · 2026Article
- IFN-γ-Driven macrophage responses in the immunity toFrontiers in cellular and infection microbiology · 2025Review
- Bacteria and macrophages in the tumor microenvironment.Frontiers in microbiology · 2023Review
- Human macrophage polarization in the response toCurrent research in microbial sciences · 2021Article
- In search of biomarkers for leprosy by unraveling the host immune response to Mycobacterium leprae.Immunological reviews · 2021Review
- Host Immune-Metabolic Adaptations Upon Mycobacterial Infections and Associated Co-Morbidities.Frontiers in immunology · 2021Review
- Poor stimulation of bovine dendritic cells byInnate immunity · 2020Article
- Hacking the host: exploitation of macrophage polarization by intracellular bacterial pathogens.Pathogens and disease · 2020Review
- Functional aspects, phenotypic heterogeneity, and tissue immune response of macrophages in infectious diseases.Infection and drug resistance · 2019Article
- BCG and Adverse Events in the Context of Leprosy.Frontiers in immunology · 2018Article
- Host Lipid Mediators in Leprosy: The Hypothesized Contributions to Pathogenesis.Frontiers in immunology · 2018Review
- Mycobacterial Phenolic Glycolipids Selectively Disable TRIF-Dependent TLR4 Signaling in Macrophages.Frontiers in immunology · 2018Article
- Leprosy As a Complex Infection: Breakdown of the Th1 and Th2 Immune Paradigm in the Immunopathogenesis of the Disease.Frontiers in immunology · 2017Review
- A curated compendium of monocyte transcriptome datasets of relevance to human monocyte immunobiology research.F1000Research · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMacrophages play a central role in the pathogenesis of leprosy, caused by Mycobacterium leprae. The polarized clinical presentations in leprosy are associated with differential immune activation. In tuberculoid leprosy, macrophages show a classical activation phenotype (M1), while macrophages in lepromatous disease display characteristics of alternative activation (M2). Bacille Calmette-Guérin (BCG) vaccination, which protects against leprosy, can promote sustained changes in monocyte response to unrelated pathogens and may preferentially direct monocytes towards an M1 protective phenotype. We previously reported that M. leprae can dampen the response of naïve human monocytes to a strong inducer of pro-inflammatory cytokines, such as BCG. Here, we investigated the ability of the pathogen to alter the direction of macrophage polarization and the impact of BCG vaccination on the monocyte response to M. leprae.
findingsWe show that in vitro exposure of monocytes from healthy donors to M. leprae interferes with subsequent M1 polarization, indicated by lower levels of M1-associated cytokine/chemokines released and reduced expression of M1 cell surface markers. Exposure to M. leprae phenolic glycolipid (PGL) 1, instead of whole bacteria, demonstrated a similar effect on M1 cytokine/chemokine release. In addition, we found that monocytes from 10-week old BCG-vaccinated infants released higher levels of the pro-inflammatory cytokines TNF-α and IL-1β in response to M. leprae compared to those from unvaccinated infants.
conclusionExposure to M. leprae has an inhibitory effect on M1 macrophage polarization, likely mediated through PGL-1. By directing monocyte/macrophages preferentially towards M1 activation, BCG vaccination may render the cells more refractory to the inhibitory effects of subsequent M. leprae infection.
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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.