Neutrophils in innate host defense against Staphylococcus aureus infections
Open accessAbstract
Staphylococcus aureus has been an important human pathogen throughout history and is currently a leading cause of bacterial infections worldwide. S. aureus has the unique ability to cause a continuum of diseases, ranging from minor skin infections to fatal necrotizing pneumonia. Moreover, the emergence of highly virulent, drug-resistant strains such as methicillin-resistant S. aureus in both healthcare and community settings is a major therapeutic concern. Neutrophils are the most prominent cellular component of the innate immune system and provide an essential primary defense against bacterial pathogens such as S. aureus. Neutrophils are rapidly recruited to sites of infection where they bind and ingest invading S. aureus, and this process triggers potent oxidative and non-oxidative antimicrobial killing mechanisms that serve to limit pathogen survival and dissemination. S. aureus has evolved numerous mechanisms to evade host defense strategies employed by neutrophils, including the ability to modulate normal neutrophil turnover, a process critical to the resolution of acute inflammation. Here we provide an overview of the role of neutrophils in host defense against bacterial pathogens and discuss strategies employed by S. aureus to circumvent neutrophil function.
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At the site of infection, neutrophils bind and ingest invading micro-organisms by phagocytosis.
“At the site of infection, neutrophils bind and ingest the invading micro-organisms by phagocytosis.”
From Superoxide Anion Chemistry—Its Role at the Core of the Innate Immunity (2023) · cites this paper as [209]
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Myeloid-Derived Suppressor Cells Contribute to Staphylococcus aureus Orthopedic Biofilm Infection
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ω-Hydroxyemodin Limits Staphylococcus aureus Quorum Sensing-Mediated Pathogenesis and Inflammation
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Staphylococcus aureus Elaborates Leukocidin AB To Mediate Escape from within Human Neutrophils
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Neutrophil Recruitment to Lymph Nodes Limits Local Humoral Response to Staphylococcus aureus
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- Authors
- Rigby, K. M., & DeLeo, F. R.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- DeLeo, Frank R.
- ORCID
- DeLeo, Frank R.
- Venue
- Seminars in Immunopathology
- Published
- 2011-11-12
- Volume
- 34
- Issue
- 2
- Pages
- 237-259
- ISSN
- 1863-2297 (ISSN-L)
- 1863-2300
- PMC
- PMC3271231
- OpenAlex
- W1990621187
- Cited by
- 400
- References
- 311
- Citations by year
- 2026: 17 · 2025: 20 · 2024: 25 · 2023: 31 · 2022: 29 · 2021: 20 · 2020: 22 · 2019: 33 · 2018: 30 · 2017: 28 · 2016: 30 · 2015: 31 · 2014: 40 · 2013: 36 · 2012: 8
- FWCI
- 2.41
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Seminars in Immunopathology (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Keywords
- neutrophils, Staphylococcus aureus, innate immunity, host defense, methicillin-resistant Staphylococcus aureus, bacterial virulence, neutrophil turnover, oxidative killing, necrotizing pneumonia, skin infections
- MeSH terms
- Animals, Anti-Infective Agents, Humans, Immunity, Innate, Neutrophils, Staphylococcal Infections, Staphylococcus aureus, Virulence, Host-Pathogen Interactions, Methicillin-Resistant Staphylococcus aureus, Immune Evasion
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