Evidence map›Paper›PMID 24247196›Full record

ArticleJournal of innate immunity2014

Sepsis-induced potentiation of peritoneal macrophage migration is mitigated by programmed cell death receptor-1 gene deficiency.

Alfred Ayala, Gwendolyn F Elphick, Ye Sul Kim, Xin Huang, Arnaldo Carreira-Rosario, Sadella C Santos, Nicholas J Shubin, Yaping Chen, Jonathan Reichner, Chun-Shiang Chung

Open access · bronzeAbstract read
In one paragraph

Article in Journal of innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

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  14. Contribution of programmed cell death receptor (PD)-1 to Kupffer cell dysfunction in murine polymicrobial sepsis.American journal of physiology. Gastrointestinal and liver physiology · 2016
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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

10 authors at 2 institutions in 1 country.

Alfred AyalaDepartment of Surgery, Division of Surgical Research, the Alpert School of Medicine at Brown University/Rhode Island Hospital, Providence, R.I., USA.
Gwendolyn F Elphick
Ye Sul Kim
Xin Huang
Arnaldo Carreira-Rosario
Sadella C Santos
Nicholas J Shubin
Yaping Chen
Jonathan Reichner
Chun-Shiang Chung
Brown University · USRhode Island Hospital · US

Funding

DIFFERENTIAL EFFECTS OF SEPSIS ON MACROPHAGE FUNCTIONR01GM046354 · NIGMS · RHODE ISLAND HOSPITAL (PROVIDENCE, RI) · PI AYALA, ALFRED · 1999 to 2016
$4.5M
Trauma and Inflammation Research TrainingT32GM065085 · NIGMS · RHODE ISLAND HOSPITAL · PI Alfred Ayala · 2004 to 2026
$3.2M
Regulatory Mechanisms of Acute Lung InjuryR01HL073525 · NHLBI · RHODE ISLAND HOSPITAL (PROVIDENCE, RI) · PI AYALA, ALFRED · 2003 to 2011
$2.9M
Short-Term Training Program to Increase Diversity in Health-Related ResearchR25HL088992 · NHLBI · BROWN UNIVERSITY · PI ABID, RUHUL, DIAZ, JOSEPH A · 2007 to 2024
$1.9M
Co-Inhibitory Molecules and the Pathology of Indirect-Acute Lung InjuryR01GM107149 · NIGMS · RHODE ISLAND HOSPITAL · PI AYALA, ALFRED · 2013 to 2015
$906k
DIFFERENTIAL EFFECTS OF SEPSIS ON MACROPHAGE FUNCTIONR29GM046354 · NIGMS · RHODE ISLAND HOSPITAL (PROVIDENCE, RI) · PI AYALA, ALFRED · 1992 to 1996
–
DIFFERENTIAL EFFECTS OF SEPSIS ON MACROPHAGE FUNCTIONR55GM046354 · NIGMS · MICHIGAN STATE UNIVERSITY · PI AYALA, ALFRED · 1991 to 1991
–
NHLBI NIH HHS HL107149NHLBI NIH HHS R01 HL073525NHLBI NIH HHS R25 HL088992NIGMS NIH HHS GM46354NIGMS NIH HHS R01 GM046354NIGMS NIH HHS R01 GM107149NIGMS NIH HHS T32 GM065085NIGMS NIH HHS T32-GM65085
6 · The paper itself

Abstract

The effect of programmed cell death receptor-1 (PD-1) on phagocyte function has not been extensively described. Here we report that experimental mouse sepsis, cecal ligation and puncture (CLP), induced a marked increase in peritoneal macrophage random migration, motility and cell spread, but these changes were lost in the absence of PD-1. Alternatively, phagocytic activity was inversely affected. In vitro cell culture imaging studies, with the macrophage cell line J774, documented that blocking PD-1 with antibody led to aggregation of the cytoskeletal proteins α-actinin and F-actin. Further experiments looking at ex vivo peritoneal macrophages from mice illustrated that a similar pattern of α-actinin and F-actin was evident on cells from wild-type CLP mice but not PD-1-/- CLP mouse cells. We also observed that fMLP-induced migration by J774 cells was markedly attenuated using PD-1 blocking antibodies, a nonselective phosphatase inhibitor and a selective Ras-related protein 1 inhibitor. Finally, peritoneal macrophages derived from CLP as opposed to Sham mice demonstrated aspects of both cell surface co-localization with CD11b and internalization of PD-1 within vacuoles independent of CD11b staining. Together, we believe the data support a role for PD-1 in mediating aspects of innate macrophage immune dysfunction during sepsis, heretofore unappreciated.

Indexed as

ActininActinsAnimalsAntibodies, BlockingCD11b AntigenCecumCell LineCell MovementDisease Models, AnimalHumansImmunity, InnateMacrophage ActivationMacrophages, PeritonealMaleMice, Inbred C57BLMice, KnockoutActininActinsAntibodies, BlockingCD11b AntigenPdcd1 protein, mouseProgrammed Cell Death 1 Receptor

Identifiers

PMID24247196
PMCPMC3972305
OpenAlexW2005965937

What OpenQuestion holds

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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.