ArticleJournal of leukocyte biology2019
Frontline Science: Staphylococcus aureus promotes receptor-interacting protein kinase 3- and protease-dependent production of IL-1β in human neutrophils.
Article in Journal of leukocyte biology, 2019. 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, 29 citations in OpenAlex.
- Adenovirus phagocytosis by neutrophils triggers a pro-inflammatory response.PLoS pathogens · 2026Article
- Context-dependent roles of the NLRP3 inflammasome in osteomyelitis and strategies for precision modulation.Frontiers in immunology · 2026Review
- Neutrophil extracellular traps and interleukin-1β in cystic fibrosis lung disease.Frontiers in immunology · 2025Review
- Article
- Effects of neutrophil fate on inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Regulated cell death in neutrophils: From apoptosis to NETosis and pyroptosis.Seminars in immunology · 2023Review
- NADPH oxidase 2 limits amplification of IL-1β-G-CSF axis and an immature neutrophil subset in murine lung inflammation.Blood advances · 2023Article
- Pyroptosis in neutrophils: Multimodal integration of inflammasome and regulated cell death signaling pathways.Immunological reviews · 2023Review
- Immunogenic cell death as driver of autoimmunity in granulomatosis with polyangiitis.Frontiers in immunology · 2022Review
- Targeting Neutrophils for Promoting the Resolution of Inflammation.Frontiers in immunology · 2022Review
- Dysregulation of neutrophil death in sepsis.Frontiers in immunology · 2022Review
- The potential value of plasma receptor interacting protein 3 in neonates with culture-positive late-onset sepsis.BMC infectious diseases · 2021Article
- Modulation of phagocytosis-induced cell death of human neutrophils by Neisseria gonorrhoeae.Journal of leukocyte biology · 2020Article
- Acute IL-4 Governs Pathogenic T Cell Responses duringImmunoHorizons · 2020Article
- Neutrophil heterogeneity and fate in inflamed tissues: implications for the resolution of inflammation.American journal of physiology. Cell physiology · 2020Article
- Involvement of caspase-1 in inflammasomes activation and bacterial clearance in S. aureus-infected osteoblast-like MG-63 cells.Cellular microbiology · 2020Article
- Article
- Pulmonary Pathogens Adapt to Immune Signaling Metabolites in the Airway.Frontiers in immunology · 2020Review
- Cell intrinsic functions of neutrophils and their manipulation by pathogens.Current opinion in immunology · 2019Review
- Protective Role of Peroxiredoxin I in Heat-KilledIn vivo (Athens, Greece)Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
Microbial infection elicits robust immune responses that initially depend on polymorphonuclear neutrophils (PMN), which ingest and kill invading bacteria. However, community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) remain viable within PMN and prompt their lysis with concomitant release of damage-associated molecular patterns and proinflammatory cytokines that promote additional inflammation. Here, we show that ultrapure human PMN (>99.8% pure) that have ingested CA-MRSA released interleukin (IL)-1β but not IL-18. The ingested CA-MRSA needed to be viable, and phagocytosis alone was insufficient to stimulate IL-1β secretion from PMN fed CA-MRSA. In contrast to PMN response to the canonical NLRP3 inflammasome agonist nigericin, IL-1β secretion by PMN fed CA-MRSA occurred independently of NLRP3 inflammasome or caspase-1 activation and required instead active receptor-interacting protein kinase 3 (RIPK3) but not RIPK1. Furthermore, inhibition of neutrophil serine proteases blocked pro-IL-1β cleavage in PMN fed CA-MRSA. Taken together, our data suggest that with respect to secretion of IL-1β and IL-18, PMN differ from human macrophages and exhibit agonist-specific responses. After phagocytosis of CA-MRSA, human PMN secreted IL-1β through a previously unrecognized mechanism dependent on RIPK3 and serine proteases but independent of canonical NLRP3 inflammasome and caspase-1 activation.
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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.