ArticleRespiratory research2010
Legionella pneumophila induces cathepsin B-dependent necrotic cell death with releasing high mobility group box1 in macrophages.
Article in Respiratory research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- The Ambiguous Role of HMGB1 Across the Hallmarks of Aging: A Narrative Review.Clinical interventions in aging · 2025Review
- Resistance of hypervirulentFrontiers in immunology · 2023Article
- The relationship between HMGB1 and autophagy in the pathogenesis of diabetes and its complications.Frontiers in endocrinology · 2023Review
- Article
- Crystalline silica induces macrophage necrosis and causes subsequent acute pulmonary neutrophilic inflammation.Cell biology and toxicology · 2022Article
- HMGB1 downregulation in retinal pigment epithelial cells protects against diabetic retinopathy through the autophagy-lysosome pathway.Autophagy · 2022Article
- The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022Review
- Review: The role of HMGB1 in spinal cord injury.Frontiers in immunology · 2022Review
- Cell death as part of innate immunity: Cause or consequence?Immunology · 2021Review
- Association of plasma level of high-mobility group box-1 with necroptosis and sepsis outcomes.Scientific reports · 2021Article
- Extracellular HMGB-1 activates inflammatory signaling in tendon cells and tissues.Therapeutic advances in chronic disease · 2020Article
- Modulation of Death and Inflammatory Signaling in Decidual Stromal Cells following Exposure to Group BInfection and immunity · 2019Article
- OtopathogenicFrontiers in microbiology · 2016Article
- Streptolysin S Promotes Programmed Cell Death and Enhances Inflammatory Signaling in Epithelial Keratinocytes during Group A Streptococcus Infection.Infection and immunity · 2015Article
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
- Legionella dumoffii utilizes exogenous choline for phosphatidylcholine synthesis.International journal of molecular sciences · 2014Article
- The expression of HMGB1 on microparticles released during cell activation and cell death in vitro and in vivo.Molecular medicine (Cambridge, Mass.) · 2014Review
- Article
- The role of high mobility group box-1 on the development of diabetes complications: A plausible pharmacological target.Diabetes & vascular disease researchReview
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLegionella pneumophila (LPN) can cause a lethal infectious disease with a marked inflammatory response in humans. However, the mechanism of this severe inflammation remains poorly understood. Since necrosis is known to induce inflammation, we investigated whether LPN induces necrosis in macrophages. We also analyzed the involvement of lysosomal cathepsin B in LPN-induced cell death.
methodsThe human monocytic cell line THP-1 was infected with LPN, NUL1 strain. MG132-treated cells were used as apoptotic control cells. After infection, the type of cell death was analyzed by using microscopy, LDH release and flow cytometry. As a proinflammatory mediator, high-mobility group box 1 (HMGB-1), was measured. Cathepsin B activity was also measured and the inhibitory effects of cathepsin B on LPN-induced cell death were analyzed.
resultsTHP-1 cells after treatment with high dose of LPN showed necrotic features with releasing HMGB-1. This necrosis and the HMGB-1 release were inhibited by a specific lysosomal cathepsin B inhibitor and were characterized by a rapid and high activation of cathepsin B that was not observed in apoptotic control cells. The necrosis was also accompanied by cathepsin B-dependent poly(ADP-ribose) polymerase (PARP) cleavage.
conclusionsWe demonstrate here that L. pneumophila rapidly induces cathepsin B-dependent necrosis in a dose-dependent manner and releases a proinflammatory mediator, HMGB-1, from macrophages. This report describes a novel aspect of the pathogenesis of Legionnaires' disease and provides a possible therapeutic target for the regulation of inflammation.
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