ArticlePLoS pathogens2015
Staphylococcus aureus Leukocidin A/B (LukAB) Kills Human Monocytes via Host NLRP3 and ASC when Extracellular, but Not Intracellular.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 128 citations in OpenAlex.
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- Zoonotic potential of methicillin-resistant Staphylococcus aureus isolated from pets and their owners in Bangladesh.Scientific reports · 2025Article
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- Immune dysfunction during S. aureus biofilm-associated implant infections: opportunities for novel therapeutic strategies.NPJ biofilms and microbiomes · 2025Review
- Enterotoxigenic Escherichia coli heat-labile enterotoxin induces cell death and disrupts effector functions in porcine monocytes.Veterinary research · 2025Article
- Hydroxy-selenomethionine helps cows to overcome heat stress by enhancing antioxidant capacity and alleviating blood-milk barrier damage.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2025Article
- Deletion of the E3 ubiquitin ligase LRSAM1 fosters intracellularFrontiers in cellular and infection microbiology · 2025Article
- NLRP3 Inflammasomes: Dual Function in Infectious Diseases.Journal of immunology (Baltimore, Md. : 1950) · 2024Review
- G protein-coupled estrogen receptor agonist G-1 decreases ADAM10 levels and NLRP3-inflammasome component activation in response to Staphylococcus aureus alpha-hemolysin.MicrobiologyOpen · 2024Article
- Strategies of bacterial detection by inflammasomes.Cell chemical biology · 2024Review
- The NLRP3 Inflammasome Is Dispensable in Methicillin-ResistantPathogens (Basel, Switzerland) · 2024Article
- TLR4 sensing of IsdB ofmBio · 2024Article
- Molecular Characteristics and Pathogenicity ofInternational journal of molecular sciences · 2023Review
- Staphylococcal protein A modulates inflammation by inducing interferon signaling in human nasal epithelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
25 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Staphylococcus aureus infections are a growing health burden worldwide, and paramount to this bacterium's pathogenesis is the production of virulence factors, including pore-forming leukotoxins. Leukocidin A/B (LukAB) is a recently discovered toxin that kills primary human phagocytes, though the underlying mechanism of cell death is not understood. We demonstrate here that LukAB is a major contributor to the death of human monocytes. Using a variety of in vitro and ex vivo intoxication and infection models, we found that LukAB activates Caspase 1, promotes IL-1β secretion and induces necrosis in human monocytes. Using THP1 cells as a model for human monocytes, we found that the inflammasome components NLRP3 and ASC are required for LukAB-mediated IL-1β secretion and necrotic cell death. S. aureus was shown to kill human monocytes in a LukAB dependent manner under both extracellular and intracellular ex vivo infection models. Although LukAB-mediated killing of THP1 monocytes from extracellular S. aureus requires ASC, NLRP3 and the LukAB-receptor CD11b, LukAB-mediated killing from phagocytosed S. aureus is independent of ASC or NLRP3, but dependent on CD11b. Altogether, this study provides insight into the nature of LukAB-mediated killing of human monocytes. The discovery that S. aureus LukAB provokes differential host responses in a manner dependent on the cellular contact site is critical for the development of anti-infective/anti-inflammatory therapies that target the NLRP3 inflammasome.
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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.