CoChat
Sign Up
Cited by 563Antimicrobial Resistance in StaphylococcusNeutrophil, Myeloperoxidase and Oxidative MechanismsStreptococcal Infections and Treatments

The DOI matches its Crossref record; 57 of the 58 references it cites were found in a registry or an index.

Insights into Mechanisms Used by Staphylococcus aureus to Avoid Destruction by Human Neutrophils

Voyich, Jovanka M, Braughton, Kevin R, Sturdevant, Daniel E, Whitney, Adeline R, Saïd-Salim, Battouli, Porcella, Stephen F, Long, R Daniel, Dorward, David W, Gardner, Donald J, Kreiswirth, Barry N, Musser, James M, DeLeo, Frank R·2005·The Journal of Immunology
DOI 10.4049/jimmunol.175.6.3907
Open this paper in CoChat — free account

Abstract

Polymorphonuclear leukocytes (PMNs, or neutrophils) are critical for human innate immunity and kill most invading bacteria. However, pathogens such as Staphylococcus aureus avoid destruction by PMNs to survive, thereby causing human infections. The molecular mechanisms used by pathogens to circumvent killing by the immune system remain largely undefined. To that end, we studied S. aureus pathogenesis and bacteria-PMN interactions using strains originally isolated from individuals with community-acquired (CA) and hospital-acquired infections. Compared with strains from hospital infections (COL and MRSA252), strain MW2 and a methicillin-susceptible relative, MnCop, were significantly more virulent in a mouse model of S. aureus infection, and caused the greatest level of pathology in major vital organs. Although phagocytosis of each strain triggered production of reactive oxygen species and granule-phagosome fusion, those from CA infections were significantly more resistant to killing by human PMNs and caused greater host cell lysis. Microarray analysis of the strains during neutrophil phagocytosis identified genes comprising a global S. aureus response to human innate host defense. Genes involved in capsule synthesis, gene regulation, oxidative stress, and virulence, were up-regulated following ingestion of the pathogen. Notably, phagocytosis of strains from CA infections induced changes in gene expression not observed in the other strains, including up-regulation of genes encoding virulence factors and hypothetical proteins. Our studies reveal a gene transcription program in a prominent human pathogen that likely contributes to evasion of innate host defense.

Overview

Integrity signals

Registry

Crossref · 10.4049/jimmunol.175.6.3907

Cites

57 of 57 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

Citations

Cites

Flagged first, then by citations

1 of the 58 references couldn’t be matched to a known paper.

Research works printed but not linked: 56

  1. 1998, N. Engl. J. Med., 520
  2. 2003, Infect. Control Hosp. Epidemiol., 451
  3. 2000, Clin. Microbiol. Rev., 16
  4. 2004, Proc. Natl. Acad. Sci. USA, 12312
  5. 2002, Lancet, 1819
  6. 2001, Proc. Natl. Acad. Sci. USA, 8821
  7. 1999, J. Am. Med. Assoc., 1123
  8. 1989, Am. J. Dis. Child., 848
  9. 2005, N. Engl. J. Med., 1445
  10. 2005, N. Engl. J. Med., 468
  11. 2004, Clin. Infect. Dis., 1446
  12. 2005, Clin. Infect. Dis., 100
  13. 2004, Proc. Natl. Acad. Sci. USA, 9786
  14. 1979, Infect. Immun., 902
  15. 1998, J. Am. Med. Assoc., 593
  16. 2003, J. Clin. Microbiol., 5113
  17. 2003, Proc. Natl. Acad. Sci. USA, 10948
  18. 1999, J. Immunol., 6732
  19. 2003, Proc. Natl. Acad. Sci. USA, 1996
  20. 2002, Lancet, 753
  21. 2000, J. Immunol., 3713
  22. 2003, FEBS Lett., 54
  23. 2004, Clin. Microbiol. Rev., 218
  24. 2003, J. Bacteriol., 6686
  25. 2003, Mol. Microbiol., 1429
  26. 2003, Mol. Microbiol., 807
  27. 2004, FEMS Immunol. Med. Microbiol., 1
  28. 2004, J. Bacteriol., 3029
  29. 2000, J. Bacteriol., 4822
  30. 2000, Trends Microbiol., 274
  31. 2002, Proc. Natl. Acad. Sci. USA, 6901
  32. 2003, J. Leukocyte Biol., 315
  33. 2003, J. Immunol., 3357
  34. 2004, J. Immunol., 636
  35. 2004, Biochem. Soc. Trans., 474
  36. 2005, N. Engl. J. Med., 1485
  37. 2005, N. Engl. J. Med., 1436
  38. 2003, J. Am. Med. Assoc., 2976
  39. 2003, Emerg. Infect. Dis., 978
  40. 2001, Clin. Infect. Dis., 990
  41. 2004, J. Clin. Microbiol., 5673
  42. 2001, J. Am. Med. Assoc., 1201
  43. 1999, Clin. Infect. Dis., 797
  44. 2000, N. Engl. J. Med., 1703
  45. 1930, J. Am. Med. Assoc., 780
  46. 1966, Ann. Intern. Med., 328
  47. 1979, Medicine (Baltimore)., 128
  48. 1976, Am. J. Med., 849
  49. 2000, Infect. Immun., 6162
  50. 1997, Infect. Immun., 2517
  51. 2004, J. Immunol., 1194
  52. 2004, J. Clin. Invest., 1732
  53. 2004, J. Clin. Microbiol., 3752
  54. 2002, Clin. Infect. Dis., 819
  55. 2005, J. Clin. Microbiol., 3373
  56. 2004, Microbes. Infect., 1117

Cited by

Sorted by citations

See all 563

Related

See all

Metadata

Authors
Voyich, J. M., Braughton, K. R., Sturdevant, D. E., Whitney, A. R., Saïd-Salim, B., Porcella, S. F., Long, R. D., Dorward, D. W., Gardner, D. J., Kreiswirth, B. N., Musser, J. M., & DeLeo, F. R.
Affiliations
  • National Institutes of Health (US)
  • Public Health Research Institute Tuberculosis Center, International Center for Public Health , Newark, NJ 07103
  • International Center for Public Health (US)
  • Baylor College of Medicine (US)
ORCID
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2005-09
Volume
175
Issue
6
Pages
3907-3919
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.175.6.3907
OpenAlex
W1848320945
Cited by
563
References
58
Citations by year
2026: 5 · 2025: 17 · 2024: 25 · 2023: 10 · 2022: 20 · 2021: 16 · 2020: 17 · 2019: 23 · 2018: 29 · 2017: 34 · 2016: 29 · 2015: 31 · 2014: 33 · 2013: 49 · 2012: 43
FWCI
12.79
Type
journal article
Language
en
Open access
closed
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institutes of Health
Topics
  • Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Health Sciences › Medicine › Infectious Diseases › Streptococcal Infections and Treatments
Keywords
Staphylococcus aureus, polymorphonuclear leukocytes, innate immunity, phagocytosis, community-acquired infections, nosocomial infections, virulence, capsule synthesis, oxidative stress, gene expression response, virulence factors, methicillin-resistant Staphylococcus aureus, host-pathogen interaction
MeSH terms
Genes, Bacterial, Humans, Immunity, Innate, Neutrophils, Phagocytosis, Staphylococcal Infections, Staphylococcus aureus, Gene Expression Regulation, Bacterial, Gene Expression Profiling, Virulence Factors

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