Evidence map›Paper›PMID 30833100›Full record

ArticleBurns : journal of the International Society for Burn Injuries2019

One-hit wonder: Late after burn injury, granulocytes can clear one bacterial infection but cannot control a subsequent infection.

Laurel B Kartchner, Cindy J Gode, Julia L M Dunn, Lindsey I Glenn, Danté N Duncan, Matthew C Wolfgang, Bruce A Cairns, Robert Maile

Open access · greenAbstract read
In one paragraph

Article in Burns : journal of the International Society for Burn Injuries, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Determination of Burn Size in Mouse Models of Burn Injury: A Scoping Review of Studies Leveraging Scald and Contact Burns.Journal of burn care & research : official publication of the American Burn Association · 2025
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Innate Immune System Response to Burn Damage-Focus on Cytokine Alteration.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
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

8 authors at 1 institution in 1 country.

Laurel B KartchnerDepartment of Microbiology and Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Cindy J GodeDepartment of Microbiology and Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Marsico Lung Institute/Cystic Fibrosis Research Center, USA.
Julia L M DunnDepartment of Microbiology and Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Lindsey I GlennDepartment of Surgery, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Danté N DuncanDepartment of Microbiology and Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Department of Surgery, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Matthew C WolfgangDepartment of Microbiology and Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Marsico Lung Institute/Cystic Fibrosis Research Center, USA.
Bruce A CairnsDepartment of Microbiology and Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Department of Surgery, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Jaycee Burn Center, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Robert MaileDepartment of Microbiology and Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Department of Surgery, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Jaycee Burn Center, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. Electronic address: robert_maile@med.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
Role of extraceullar vesicles in directing immunometabolic homeostasis after burn injuryR01GM131124 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CAIRNS, BRUCE A, MAILE, ROBERT · 2019 to 2022
$1.5M
Cellular mechanism of immune dysfunction following burn injuryR01GM076250 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CAIRNS, BRUCE A · 2009 to 2013
$1.5M
NCI NIH HHS P30 CA016086NIGMS NIH HHS R01 GM076250NIGMS NIH HHS R01 GM131124
6 · The paper itself

Abstract

objectiveBurn injury induces an acute hyperactive immune response followed by a chronic immune dysregulation that leaves those afflicted susceptible to multiple secondary infections. Many murine models are able to recapitulate the acute immune response to burn injury, yet few models are able to recapitulate long-term immune suppression and thus chronic susceptibility to bacterial infections seen in burn patients. This has hindered the field, making evaluation of the mechanisms responsible for these susceptibilities difficult to study. Herein we describe a novel mouse model of burn injury that promotes chronic immune suppression allowing for susceptibility to primary and secondary infections and thus allows for the evaluation of associated mechanisms.

methodsC57Bl/6 mice receiving a full-thickness contact burn were infected with Pseudomonas aeruginosa 14 days (primary infection) and/or 17 days (secondary infection) after burn or sham injury. The survival, pulmonary and systemic bacterial load as well as frequency and function of innate immune cells (neutrophils and macrophages) were evaluated.

resultsFollowing secondary infection, burn mice were less effective in clearance of bacteria compared to sham injured or burn mice following a primary infection. Following secondary infection both neutrophils and macrophages recruited to the airways exhibited reduced production of anti-bacterial reactive oxygen and nitrogen species and the pro-inflammatory cytokineIL-12 while macrophages demonstrated increased expression of the anti-inflammatory cytokine interleukin-10 compared to those from sham burned mice and/or burn mice receiving a primary infection. In addition the BALF from these mice contained significantly higher level so of the anti-inflammatory cytokine IL-4 compared to those from sham burned mice and/or burn mice receiving a primary infection.

conclusionsBurn-mediated protection from infection is transient, with a secondary infection inducing immune protection to collapse. Repeated infection leads to increased neutrophil and macrophage numbers in the lungs late after burn injury, with diminished innate immune cell function and an increased anti-inflammatory cytokine environment.

Indexed as

AnimalsBacterial InfectionsBacterial LoadBronchoalveolar Lavage FluidBurnsDisease Models, AnimalImmune ToleranceImmunocompromised HostInterleukin-10Interleukin-12Interleukin-4LungMacrophagesMiceNeutrophilsPneumonia, BacterialInterleukin-10Interleukin-12Interleukin-4Reactive Nitrogen SpeciesReactive Oxygen SpeciesBurnGranulocytesMacrophagesNeutrophilsPseudomonas

Identifiers

PMID30833100
PMCPMC6482098
OpenAlexW2918507079

What OpenQuestion holds

Textmetadata
LicenceTDM
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.