Evidence map›Paper›PMID 29345058›Full record

ArticleJournal of leukocyte biology2018

Frontline Science: Anti-PD-L1 protects against infection with common bacterial pathogens after burn injury.

Naeem K Patil, Liming Luan, Julia K Bohannon, Antonio Hernandez, Yin Guo, Edward R Sherwood

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. A comparativeFrontiers in cellular and infection microbiology · 2023
    Article
  11. Article
  12. Innate Immune System Response to Burn Damage-Focus on Cytokine Alteration.International journal of molecular sciences · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Observational
  17. Review
  18. Eosinophils and Bacteria, the Beginning of a Story.International journal of molecular sciences · 2021
    Review
  19. Observational
  20. PD-L1Science advances · 2021
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Naeem K PatilDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Liming LuanDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Julia K BohannonDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Antonio HernandezDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Yin GuoDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Edward R SherwoodDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Vanderbilt University Medical Center · US

Funding

Resistance of Beta 2 Microglobulin Null Mice to SepsisR01GM066885 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SHERWOOD, EDWARD R · 2003 to 2016
$4.4M
Enhancing Resistance to Infection after Burn Injury with TLR AgonistsR01GM121711 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BOHANNON, JULIA K. · 2017 to 2021
$1.6M
Enhancement of Innate Anti-Microbial Immunity Using Novel Synthetic TLR4 AgonistsK08GM123345 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HERNANDEZ, ANTONIO · 2017 to 2020
$699k
NIGMS NIH HHS R01 GM066885NIGMS NIH HHS R01 GM121711
6 · The paper itself

Abstract

Burn patients are susceptible to infections due, in part, to immune dysfunction. Upregulation of programmed death-1 (PD-1) receptor on T cells and programmed cell death ligand-1 (PD-L1) on myeloid cells contribute to immune dysfunction in nonburn-related sepsis. We hypothesized that PD-1/PDL1 interactions contribute to immune dysfunction after burn injury. To determine the impact of burn injury and infection on PD-L1, PD-1 and costimulatory receptor expression by leukocytes and its relationship to T cell functions. The efficacy of anti-PD-L1 antibody was evaluated in a clinically relevant mouse model of burn injury and bacterial infection. Mice underwent 35% scald burn followed by Pseudomonas aeruginosa or Staphylococcus aureus infection on day 4 postburn. Anti-PD-L1 was administered on day 3 postburn. Numbers and phenotype of leukocytes, plasma cytokine concentrations, bacterial clearance, organ injury, and survival were assessed. Burn injury and infection with P. aeruginosa caused a significant upregulation of PD-L1 on myeloid cells, along with a decrease in T cell numbers and function, significant multiorgan injury, and decreased survival. Treatment with anti-PD-L1 antibody improved bacterial clearance, reduced organ injury, and enhanced survival during Pseudomonas burn wound infection. Furthermore, anti-PD-L1 effectively protected against multiorgan injury, and improved bacterial clearance and survival following systemic S. aureus infection after burn injury. Blockade of PD-1/PD-L1 interactions might represent a viable treatment to improve outcomes among critically ill burn-injured subjects and increased leukocyte PD-L1 expression could serve as a valuable biomarker to select appropriate patients for such treatment.

Indexed as

AnimalsAntibodies, MonoclonalB7-H1 AntigenBurnsCytokinesDisease Models, AnimalMaleMiceMice, Inbred BALB CPseudomonas aeruginosaPseudomonas InfectionsStaphylococcal InfectionsStaphylococcus aureusT-LymphocytesWound InfectionAntibodies, MonoclonalB7-H1 AntigenCD274 protein, humanCytokinesburn injurycheckpoint receptorsinfectionmyeloid cellssepsisT cells

Identifiers

PMID29345058
PMCPMC9680647
OpenAlexW2780648853

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.