ArticleTuberculosis (Edinburgh, Scotland)2013
Pathways of IL-1β secretion by macrophages infected with clinical Mycobacterium tuberculosis strains.
Article in Tuberculosis (Edinburgh, Scotland), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
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- Human alveolar macrophage response to Mycobacterium tuberculosis: immune characteristics underlying large inter-individual variability.Communications biology · 2025Article
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- Decreased IL-1 β Secretion as a Potential Predictor of Tuberculosis Recurrence in Individuals Diagnosed with HIV.Biomedicines · 2024Article
- Whole-blood culture-derived cytokine combinations for the diagnosis of tuberculosis.Frontiers in immunology · 2024Article
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- Histone deacetylase-2 controls IL-1β production through the regulation of NLRP3 expression and activation in tuberculosis infection.iScience · 2022Article
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- Exploring the Use of Medicinal Plants and Their Bioactive Derivatives as Alveolar NLRP3 Inflammasome Regulators duringInternational journal of molecular sciences · 2021Review
- Blutaparon portulacoides ethanolic extract reduced IL-1β and inflammatory parameters induced by the Mycobacterium complex and carrageenan in mice.Inflammopharmacology · 2021Article
- Prophage GeneFrontiers in microbiology · 2021Article
- Simvastatin Enhances the Immune Response AgainstFrontiers in microbiology · 2019Article
- Differed IL-1 Beta Response between Active TB and LTBI Cases by Ex Vivo Stimulation of Human Monocyte-Derived Macrophage with TB-Specific Antigen.Disease markers · 2019Article
- Immunological recovery in patients with pulmonary tuberculosis after intensive phase treatment.The Journal of international medical research · 2018Article
- Heparin inhibits intracellular Mycobacterium tuberculosis bacterial replication by reducing iron levels in human macrophages.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The pro-inflammatory cytokine IL-1β is a key mediator of inflammation and plays an important role in the host resistance to Mycobacterium tuberculosis infections. To date, most studies have examined the mechanisms of IL-1β secretion using laboratory strains of M. tuberculosis and the findings may not be widely applicable to contemporary clinical strains. Here, we investigated the primary pathways of IL-1β secretion in macrophages infected with a panel of 17 clinical M. tuberculosis isolates, representing Euro-American, Indo-Oceanic and East-Asian/Beijing lineages. Our aim was to dissect the pathways involved in M. tuberculosis induced IL-1β secretion and to determine whether they are common to all clinical isolates. We found that the isolates were capable of eliciting variable concentrations of IL-1β from infected murine macrophages, but this phenomenon could not be attributed to differential IL-1β mRNA transcription or pro-IL-1β accumulation. We demonstrate that viable bacteria are required to induce IL-1β secretion from macrophages, but IL-1β secretion was only partially abrogated by caspase-1 inhibition. Almost complete IL-1β secretion inhibition was produced with combined caspase-1 and some serine protease inhibitors. Taken together, these findings demonstrate that clinical strains of M. tuberculosis employ a unique caspase-1 independent pathway to stimulate IL-1β secretion from macrophages.
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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.