ArticleMicrobiology (Reading, England)2008
A role for tumour necrosis factor-alpha, complement C5 and interleukin-6 in the initiation and development of the mycobacterial cord factor trehalose 6,6'-dimycolate induced granulomatous response.
Article in Microbiology (Reading, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
35 citing papers in PubMed, 70 citations in OpenAlex.
- WRN Nuclease-Mediated EcDNA Clearance Enhances Antitumor Therapy in Conjunction with Trehalose Dimycolate/Mesoporous Silica Nanoparticles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Modulation of TDM-induced granuloma pathology by human lactoferrin: a persistent effect in mice.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023Article
- Modulation of TDM-induced granuloma pathology by human lactoferrin: a persistent effect in mice.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023Article
- Recombinant Human Lactoferrin Reduces Inflammation and Increases Fluoroquinolone Penetration to Primary Granulomas During Mycobacterial Infection of C57Bl/6 Mice.Archivum immunologiae et therapiae experimentalis · 2022Article
- Article
- The Role of Complement System and the Immune Response to Tuberculosis Infection.Medicina (Kaunas, Lithuania) · 2021Review
- Mycobacterial Trehalose 6,6'-Dimycolate-Induced M1-Type Inflammation.The American journal of pathology · 2020Article
- Silver Nanoparticles for the Therapy of Tuberculosis.International journal of nanomedicine · 2020Review
- The sensor kinase MtrB ofThe Journal of biological chemistry · 2019Article
- Mycobacterial trehalose 6,6'-dimycolate induced vascular occlusion is accompanied by subendothelial inflammation.Tuberculosis (Edinburgh, Scotland) · 2019Article
- Underestimated Manipulative Roles ofFrontiers in immunology · 2019Review
- Oral recombinant human or mouse lactoferrin reduces Mycobacterium tuberculosis TDM induced granulomatous lung pathology.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2017Article
- Mincle-mediated translational regulation is required for strong nitric oxide production and inflammation resolution.Nature communications · 2016Article
- Granulomas and Inflammation: Host-Directed Therapies for Tuberculosis.Frontiers in immunology · 2016Review
- Mycobacteria Clumping Increase Their Capacity to Damage Macrophages.Frontiers in microbiology · 2016Article
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- Article
- Lactoferrin: A Modulator for Immunity against Tuberculosis Related Granulomatous Pathology.Mediators of inflammation · 2015Review
- The contraceptive depot medroxyprogesterone acetate impairs mycobacterial control and inhibits cytokine secretion in mice infected with Mycobacterium tuberculosis.Infection and immunity · 2013Article
- Structural determination and Toll-like receptor 2-dependent proinflammatory activity of dimycolyl-diarabino-glycerol from Mycobacterium marinum.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Trehalose 6,6'-dimycolate (TDM) is a glycolipid component of the mycobacterial cell wall that causes immune responses in mice similar to Mycobacterium tuberculosis (MTB) infection, including granuloma formation with production of proinflammatory cytokines. The precise roles of tumour necrosis factor (TNF)-alpha, complement C5 and interleukin (IL)-6 in the molecular events that lead to the initiation and maintenance of the granulomatous response to TDM have not been fully elucidated. Macrophage proinflammatory responses from wild-type and complement-deficient mice after infection with MTB were assessed, and compared to responses from organisms in which surface TDM had been removed. Removal of TDM abolished proinflammatory responses, markedly so in the complement-deficient macrophages. Mice deficient in TNF-alpha, C5a and IL-6, along with wild-type C57BL/6 controls, were intravenously injected with TDM in a water-in-oil emulsion, and analysed for histological response and cytokine production in lungs. Wild-type C57BL/6 mice formed granulomas with increased production of IL-1beta, IL-6, TNF-alpha, macrophage inflammatory protein-1alpha (MIP-1alpha), IL-12p40, interferon-gamma (IFN-gamma), and IL-10 protein and mRNA. TNF-alpha-deficient mice failed to produce a histological response to TDM, with no increases in cytokine production following TDM administration. While C5a-deficient mice exhibited inflammation, they did not form structured granulomas and initially had decreased production of proinflammatory mediators. IL-6-deficient mice initiated granuloma formation, but failed to maintain the granulomas through day 7 and demonstrated decreased early production of proinflammatory mediators in comparison to wild-type mice. These data suggest that TNF-alpha is critical for initiation of the granulomatous response, C5a is necessary for formation of cohesive granulomas, and IL-6 plays a key role in the granuloma maintenance response to mycobacterial TDM.
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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.