Evidence map›Paper›PMID 21402768›Full record

ArticleInfection and immunity2011

Participation of CD11c(+) leukocytes in methicillin-resistant Staphylococcus aureus clearance from the lung.

Francis J Martin, Dane Parker, Bryan S Harfenist, Grace Soong, Alice Prince

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Pathogens (Basel, Switzerland) · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. The Role of Macrophages inFrontiers in immunology · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Neutrophils: Beneficial and Harmful Cells in Septic Arthritis.International journal of molecular sciences · 2018
    Review
  15. Article
  16. Ablation of Pericyte-Like Cells in Lungs by Oropharyngeal Aspiration of Diphtheria Toxin.American journal of respiratory cell and molecular biology · 2017
    Article
  17. Review
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Francis J MartinDepartment of Pharmacology, Columbia University, New York, NY 10032, USA.
Dane Parker
Bryan S Harfenist
Grace Soong
Alice Prince
Columbia University · US

Funding

STAPHYLOCOCCUS AUREUS ACTIVATION OF TNF SIGNALING PATHWAYSR01HL079395 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PRINCE, ALICE S · 2006 to 2016
$4.3M
NHLBI NIH HHS 2R01HL079395NHLBI NIH HHS R01 HL079395
6 · The paper itself

Abstract

Staphylococcus aureus causes especially severe pulmonary infection, associated with high morbidity and mortality. In addition to the effects of specific virulence factors, it appears that the intensity of the host proinflammatory response, particularly in the initial stages of infection, contributes substantially to pulmonary damage. We tested the hypothesis that the CD11c(+) leukocytes are important in the host response to pulmonary infection with methicillin-resistant S. aureus (MRSA) USA300. Clodronate-induced depletion of the alveolar macrophage population resulted in increased numbers of dendritic cells (DCs) and CD4(+) cells in bronchoalveolar lavage (BAL) fluid and was associated with significantly increased mortality by 18 h following S. aureus inoculation but had no effect on bacterial load or polymorphonuclear leukocyte (PMN) numbers in the lung. These clodronate-treated mice also had increased expression of interleukin-17A/F (IL-17A/F) and CXCL10 but not of gamma interferon (IFN-γ) or tumor necrosis factor (TNF). Depletion of the dendritic cell population in mice expressing a CD11c-enhanced green fluorescent protein (EGFP)-diphtheria toxin receptor (DTR) transgene was associated with an increased bacterial load in the lung but not increased mortality. Both DCs and airway epithelial cells produced CXCL9, -10, and -11 in response to S. aureus. Pretreatment of mice with an anti-CXCR3 antibody prior to inoculation with MRSA substantially reduced CD4(+) cells and decreased pulmonary inflammation at 18 h postinfection compared to pretreatment with an IgG control. The results of these experiments suggest that CD11c(+) cells, the induction of CXCR3 ligand expression, and subsequent CD4(+) cell recruitment have an important role in the pathogenesis of severe MRSA pulmonary infection.

Indexed as

AnimalsCD11c AntigenCD4-Positive T-LymphocytesCell SeparationCytokinesEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryLeukocytesLungMaleMethicillin-Resistant Staphylococcus aureusMiceMice, Inbred C57BLMice, TransgenicReceptors, CXCR3CD11c AntigenCxcr3 protein, mouseCytokinesReceptors, CXCR3

Identifiers

PMID21402768
PMCPMC3088152
OpenAlexW2097507892

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.