Evidence map›Paper›PMID 27053759›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Resistance to Acute Macrophage Killing Promotes Airway Fitness of Prevalent Community-Acquired Staphylococcus aureus Strains.

Vijaya Kumar Yajjala, Vinai Chittezham Thomas, Christopher Bauer, Tyler D Scherr, Karl J Fischer, Paul D Fey, Kenneth W Bayles, Tammy Kielian, Keer Sun

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Article
  2. Pathogens (Basel, Switzerland) · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Age-induced prostaglandin ENature communications · 2022
    Article
  13. Article
  14. Article
  15. The Role of Macrophages inFrontiers in immunology · 2020
    Review
  16. Article
  17. Article
  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

9 authors.

Vijaya Kumar YajjalaDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198.ORCID 0000-0001-6155-1138
Vinai Chittezham ThomasDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198.ORCID 0000-0002-7886-0727
Christopher BauerDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198.
Tyler D ScherrDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198.
Karl J FischerDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198.
Paul D FeyDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198.
Kenneth W BaylesDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198.
Tammy KielianDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198.
Keer SunDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198 Keer.sun@unmc.edu.

Funding

Oxidative Burst in Influenza and MRSA Co-infectionR01HL118408 · NHLBI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI SUN, KEER · 2013 to 2022
$3.9M
NHLBI NIH HHS R01 HL118408
6 · The paper itself

Abstract

The incidence of methicillin-resistant Staphylococcus aureus (MRSA) pneumonia in otherwise healthy individuals is increasing. To investigate the mechanism underlying the epidemiological success of predominant community-associated (CA)-MRSA strains, we examined their fitness traits during the initial interaction between bacteria and the host occurring in the lower airway. Using a mouse respiratory infection model, we show that clinical isolates often responsible for CA infections are highly resistant to clearance from healthy airways, whereas S. aureus strains not as prevalent or traditionally associated with hospital-associated infections are relatively susceptible. Mechanistically, the competitive fitness of S. aureus is a result of both agr-dependent and -independent resistance to innate bacterial killing. Furthermore, we show that rather than evasion from neutrophil-dependent bactericidal process, the observed S. aureus fitness in the lower airways is due to its intrinsic resistance to resident alveolar macrophage-mediated intracellular killing. Importantly, we demonstrate that the virulence determinants responsible for bacterial persistence in immune-competent mice are dispensable in mice with predisposing conditions such as influenza infection. Taken together, these novel findings of the improved competence of predominant CA-MRSA strains to survive innate killing in healthy hosts, particularly at the very beginning stage of infection, provide a unique insight into their epidemiological success.

Indexed as

AnimalsBronchoalveolar Lavage FluidCell LineCoinfectionDNA, BacterialFemaleGenes, BacterialKaplan-Meier EstimateMacrophages, AlveolarMaleMethicillin-Resistant Staphylococcus aureusMiceMice, Inbred C57BLMicrobial Sensitivity TestsNeutrophilsOrthomyxoviridae InfectionsDNA, BacterialVirulence Factors

Identifiers

PMID27053759
PMCPMC4868659

What OpenQuestion holds

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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.