CoChat
Sign Up
Cited by 402Neutrophil, Myeloperoxidase and Oxidative MechanismsAntimicrobial Resistance in StaphylococcusInflammation biomarkers and pathways

The DOI matches its Crossref record; 314 of the 314 references it cites were found in a registry or an index.

Neutrophils in innate host defense against Staphylococcus aureus infections

Open access
Rigby, Kevin M., DeLeo, Frank R.·2012·Seminars in Immunopathology
DOI 10.1007/s00281-011-0295-3PMC PMC3271231
Open this paper in CoChat — free accountOpen PDF

Abstract

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.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1007/s00281-011-0295-3

Cites

314 of 314 references verified0 citation errors · 0 not checkable

Statistics

Figures

Fig. 1 Neutrophil emigration from vascular space to site of infection followed by phagocytosis and microbial killing. Marginating neutrophils survey post-capillary venules for signs of inflammation or invading microorganisms, undergoing transient tethering interactions with endothelial cells that facilitate neutrophil rolling along the endothelial wall and allow neutrophils to search for host- and/or microbe-derived chemotactic signals. Chemotactic molecules diffusing from the site of infection and into the bloodstream bind specific receptors on the neutrophil surface, arresting the rolling process and inducing firm adherence to the endothelial wall. Firm adherence subsequently leads to neutrophil transmigration through the endothelial wall into the tissue, a process known as extravasation. Once in the tissue, primed neutrophils chemotactically migrate to the site of infection where they recognize and phagocytose invading microorganisms. Within the phagosome of the activated neutrophil, microbes are destroyed by NADPH oxidase-derived reactive oxygen species and antimicrobial proteins released upon granule fusion with the phagosome (degranulation). See text for details. CR complement receptor, FcR Fc receptor, MPO myeloperoxidase
Fig. 1 Neutrophil emigration from vascular space to site of infection followed by phagocytosis and microbial killing. Marginating neutrophils survey post-capillary venules for signs of inflammation or invading microorganisms, undergoing transient tethering interactions with endothelial cells that facilitate neutrophil rolling along the endothelial wall and allow neutrophils to search for host- and/or microbe-derived chemotactic signals. Chemotactic molecules diffusing from the site of infection and into the bloodstream bind specific receptors on the neutrophil surface, arresting the rolling process and inducing firm adherence to the endothelial wall. Firm adherence subsequently leads to neutrophil transmigration through the endothelial wall into the tissue, a process known as extravasation. Once in the tissue, primed neutrophils chemotactically migrate to the site of infection where they recognize and phagocytose invading microorganisms. Within the phagosome of the activated neutrophil, microbes are destroyed by NADPH oxidase-derived reactive oxygen species and antimicrobial proteins released upon granule fusion with the phagosome (degranulation). See text for details. CR complement receptor, FcR Fc receptor, MPO myeloperoxidaseCC BY-NC · PubMed Central
Fig. 2 S. aureus immune evasion mechanisms and possible outcomes of bacteria–neutrophil interaction. A Immune evasion by S. aureus includes strategies that serve to prevent recognition, inhibit chemotaxis, moderate ROS, protect against AMPs, and directly damage immune cells. B Phagocytic uptake of bacteria triggers production of ROS and degranulation, working collectively to kill ingested bacteria, after which neutrophils undergo apoptosis to be removed by macrophages and promote healthy resolution of infection. Alternatively, bacterial pathogens can alter normal neutrophil turnover, promoting either a delay in neutrophil apoptosis or an accelerated neutrophil lysis. Alteration of normal neutrophil turnover facilitates pathogen survival and promotion of disease. APS antimicrobial peptide-sensing system, Aur aureolysin, CHIPS chemotaxis inhibitory protein of S. aureus, CP capsular polysaccharide, Hla α-toxin, HlgABC γ-hemolysin, LukGH LukF-G and LukS-H, MprF multiple peptide resistance factor, PIA polysaccharide intercellular adhesion, PSMs phenol-soluble modulins, PVL Panton–Valentine leukocidin, Sbi second binding protein of immunoglobulin, SCIN staphylococcal inhibitor of complement, SOD superoxide dismutase, TSST toxic shock syndrome toxin, VraFG vancomycin-resistant-associated gene, ABC transporter
Fig. 2 S. aureus immune evasion mechanisms and possible outcomes of bacteria–neutrophil interaction. A Immune evasion by S. aureus includes strategies that serve to prevent recognition, inhibit chemotaxis, moderate ROS, protect against AMPs, and directly damage immune cells. B Phagocytic uptake of bacteria triggers production of ROS and degranulation, working collectively to kill ingested bacteria, after which neutrophils undergo apoptosis to be removed by macrophages and promote healthy resolution of infection. Alternatively, bacterial pathogens can alter normal neutrophil turnover, promoting either a delay in neutrophil apoptosis or an accelerated neutrophil lysis. Alteration of normal neutrophil turnover facilitates pathogen survival and promotion of disease. APS antimicrobial peptide-sensing system, Aur aureolysin, CHIPS chemotaxis inhibitory protein of S. aureus, CP capsular polysaccharide, Hla α-toxin, HlgABC γ-hemolysin, LukGH LukF-G and LukS-H, MprF multiple peptide resistance factor, PIA polysaccharide intercellular adhesion, PSMs phenol-soluble modulins, PVL Panton–Valentine leukocidin, Sbi second binding protein of immunoglobulin, SCIN staphylococcal inhibitor of complement, SOD superoxide dismutase, TSST toxic shock syndrome toxin, VraFG vancomycin-resistant-associated gene, ABC transporterCC BY-NC · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Cited by

Sorted by citations

See all 402

Related

See all

Metadata

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
Publisher
Springer Science and Business Media LLC
Published
2011-11-12
Volume
34
Issue
2
Pages
237-259
ISSN
  • 1863-2297 (ISSN-L)
  • 1863-2300
DOI
10.1007/s00281-011-0295-3
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
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review