Evidence map›Paper›PMID 27835962›Full record

ArticleJournal of translational medicine2016

Soluble programmed cell death receptor-1 (sPD-1): a potential biomarker with anti-inflammatory properties in human and experimental acute respiratory distress syndrome (ARDS).

Sean F Monaghan, Chun-Shiang Chung, Yaping Chen, Joanne Lomas-Neira, William G Fairbrother, Daithi S Heffernan, William G Cioffi, Alfred Ayala

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  9. The role of lung macrophages in acute respiratory distress syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
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  12. lncRNA NEAT1 aggravates sepsis-induced lung injury by regulating the miR-27a/PTEN axis.Laboratory investigation; a journal of technical methods and pathology · 2021
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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.

Sean F MonaghanDivision of Surgical Research, Department of Surgery, Alpert School of Medicine at Brown University and Rhode Island Hospital, 593 Eddy Street, Providence, RI, 02903, USA. smonaghan@lifespan.org.ORCID 0000-0003-1490-3043
Chun-Shiang ChungDivision of Surgical Research, Department of Surgery, Alpert School of Medicine at Brown University and Rhode Island Hospital, 593 Eddy Street, Providence, RI, 02903, USA.
Yaping ChenDivision of Surgical Research, Department of Surgery, Alpert School of Medicine at Brown University and Rhode Island Hospital, 593 Eddy Street, Providence, RI, 02903, USA.
Joanne Lomas-NeiraDivision of Surgical Research, Department of Surgery, Alpert School of Medicine at Brown University and Rhode Island Hospital, 593 Eddy Street, Providence, RI, 02903, USA.
William G FairbrotherMCB Department, Brown University, 70 Ship Street, Providence, RI, 02903, USA.
Daithi S HeffernanDivision of Surgical Research, Department of Surgery, Alpert School of Medicine at Brown University and Rhode Island Hospital, 593 Eddy Street, Providence, RI, 02903, USA.
William G CioffiDivision of Surgical Research, Department of Surgery, Alpert School of Medicine at Brown University and Rhode Island Hospital, 593 Eddy Street, Providence, RI, 02903, USA.
Alfred AyalaDivision of Surgical Research, Department of Surgery, Alpert School of Medicine at Brown University and Rhode Island Hospital, 593 Eddy Street, Providence, RI, 02903, USA.
Brown University · US

Funding

Uncoupling of IL-1 beta and VEGF-A Crosstalk Contributes to Impaired Arteriogenesis Response to Ischemia in Chronic Diabetes MellitusP20GM103652 · NIGMS · OCEAN STATE RESEARCH INSTITUTE, INC. · PI YAO, HONGWEI · 2013 to 2022
$21.3M
Mechanisms of Immune Dysfunction and Morbid Outcome in Response to Shock/SepsisR35GM118097 · NIGMS · RHODE ISLAND HOSPITAL · PI AYALA, ALFRED · 2016 to 2025
$6.3M
Co-Inhibitory Molecules and the Pathology of Indirect-Acute Lung InjuryR01GM107149 · NIGMS · RHODE ISLAND HOSPITAL · PI AYALA, ALFRED · 2013 to 2015
$906k
Sepsis Induced Changes in iNKT-Cells and their Effect on Phagocyte FunctionK08GM110495 · NIGMS · RHODE ISLAND HOSPITAL · PI HEFFERNAN, DAVID · 2015 to 2018
$786k
NIGMS NIH HHS K08 GM110495NIGMS NIH HHS P20 GM103652NIGMS NIH HHS R01 GM107149NIGMS NIH HHS R35 GM118097
6 · The paper itself

Abstract

backgroundAcute respiratory distress syndrome (ARDS) remains a common organ dysfunction in the critically ill patient. Mechanisms for its development have focused on immune mediated causes, aspects of our understanding are not complete, and we lack biomarkers. DESIGN, SETTING, AND SUBJECTS: Blood and bronchial alveolar lavage fluid (BAL) from humans (n = 10-13) with ARDS and controls (n = 5-10) as well as a murine model of ARDS (n = 5-6) with controls (n = 6-7) were studied.

methodsARDS was induced in mice by hemorrhagic shock (day 1) followed by poly-microbial sepsis (day 2). Samples were then collected on the third day after the animals were euthanized. Ex vivo experiments used splenocytes from animals with ARDS cultured with and without soluble programmed death receptor-1 (sPD-1).

resultsLevels of sPD-1 are increased in both the serum (11,429.3 pg/mL(SD 2133.3) vs. 8061.4(SD 4187.8), p = 0.036) and bronchial alveolar lavage (BAL) fluid (6,311.1 pg/mL(SD 3758.0) vs. 90.7 pg/mL(SD 202.8), p = 0.002) of humans with ARDS. Similar results are seen in the serum (9396.1 pg/mL(SD 1546.0) vs. 3464.5 pg/mL(SD 2511.8), p = 0.001) and BAL fluid (2891.7 pg/mL(SD 868.1) vs. 1385.9 pg/mL(SD 927.8), p = 0.012) of mice. sPD-1 levels in murine blood (AUC = 1(1-1), p = 0.006), murine BAL fluid (AUC = 0.905(0.717-1.093), p = 0.015), and human BAL (AUC = 1(1-1), p = 0.001) fluid predicted ARDS. To assess the importance of sPD-1 in ARDS, ex vivo experiments were undertaken. BAL fluid from mice with ARDS dampens the TNF-α production compared to cells cultured with BAL lacking sPD-1 (2.7 pg/mL(SD 3.8) vs. 52.38 pg/mL(SD 25.1), p = 0.002).

conclusionsThis suggests sPD-1 is elevated in critical illness and may represent a potential biomarker for ARDS. In addition, sPD-1 has an anti-inflammatory mechanism in conditions of marked stress and aids in the resolution of severe inflammation. sPD-1 could be used to not only diagnose ARDS, but may be a potential therapy.

Indexed as

AnimalsAnti-Inflammatory AgentsBiomarkersBronchoalveolar Lavage FluidCD3 ComplexCells, CulturedDemographyDisease Models, AnimalFemaleHumansMaleMice, Inbred C57BLMiddle AgedProgrammed Cell Death 1 ReceptorRespiratory Distress SyndromeSolubilityAnti-Inflammatory AgentsBiomarkersCD3 ComplexProgrammed Cell Death 1 ReceptorAcute respiratory distress syndromeARDSBiomarkerImmunotherapyPD-1Soluble PD-1

Identifiers

PMID27835962
PMCPMC5106799
OpenAlexW2555902125

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Registered trials

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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.