Evidence map›Paper›PMID 21788440›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Immune unresponsiveness to secondary heterologous bacterial infection after sepsis induction is TRAIL dependent.

Prajwal Gurung, Deepa Rai, Stephanie A Condotta, Jeffrey C Babcock, Vladimir P Badovinac, Thomas S Griffith

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

46 citing papers in PubMed, 63 citations in OpenAlex.

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  10. New Insights into the Immune System Using Dirty Mice.Journal of immunology (Baltimore, Md. : 1950) · 2020
    Review
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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

6 authors at 1 institution in 1 country.

Prajwal GurungDepartment of Urology, University of Iowa, Iowa City, IA 52242, USA.
Deepa Rai
Stephanie A Condotta
Jeffrey C Babcock
Vladimir P Badovinac
Thomas S Griffith
University of Iowa · US

Funding

TRAIL-expressing Recombinant Adenovirus Based Immunotherapy for RCCR01CA109446 · NCI · UNIVERSITY OF MINNESOTA · PI GRIFFITH, THOMAS S · 2004 to 2013
$2.6M
Memory CD8 T Cell Responses After Multiple Antigen EncountersR01AI083286 · NIAID · UNIVERSITY OF IOWA · PI BADOVINAC, VLADIMIR P · 2009 to 2012
$1.5M
Apoptotic cells induce tolerance through TRAIL-expressing CD8+ regulatory T cellsR56AI077565 · NIAID · UNIVERSITY OF IOWA · PI GRIFFITH, THOMAS S · 2009 to 2009
$372k
Using microbially-experienced mice to study the innate immune response in sepsisI01BX001324 · VA · MINNEAPOLIS VA MEDICAL CENTER · PI GRIFFITH, THOMAS S · 2013 to 2025
–
BLRD VA I01 BX001324NCI NIH HHS CA109446NCI NIH HHS R01 CA109446NIAID NIH HHS AI 077565NIAID NIH HHS AI83286NIAID NIH HHS R01 AI077565NIAID NIH HHS R01 AI083286NIAID NIH HHS R56 AI077565
6 · The paper itself

Abstract

Sepsis is the leading cause of death in most intensive care units, and patients who survive the hyperinflammation that develops early during sepsis later display severely compromised immunity. Not only is there apoptosis of lymphoid and myeloid cells during sepsis that depletes these critical cellular components of the immune system, but also the remaining immune cells show decreased function. Using a cecal-ligation and puncture (CLP) model to induce intra-abdominal polymicrobial peritonitis, we recently established a link between the apoptotic cells generated during sepsis and induction of sepsis-induced suppression of delayed-type hypersensitivity. The present study extends this earlier work to include a secondary heterologous bacterial infection (OVA(257)-expressing Listeria monocytogenes [LM-OVA]) subsequent to sepsis initiation to investigate sepsis-induced alterations in the control of this secondary infection and the associated naive Ag-specific CD8 T cell response. We found that CLP-treated wild-type (WT) mice had a reduced ability to control the LM-OVA infection, which was paralleled by suppressed T cell responses, versus sham-treated WT mice. In contrast, CLP-treated Trail(-/-) and Dr5(-/-) mice were better able to control the secondary bacterial infection, and the Ag-specific CD8 T cell response was similar to that seen in sham-treated mice. Importantly, administration of a blocking anti-TRAIL mAb to CLP-treated WT mice was able to restore the ability to control the LM-OVA infection and generate Ag-specific CD8 T cell responses like those seen in sham-treated mice. These data further implicate TRAIL-dependent immune suppression during sepsis and suggest TRAIL neutralization may be a potential therapeutic target to restore cellular immunity in septic patients.

Indexed as

AnimalsCell SeparationDisease Models, AnimalFlow CytometryImmune ToleranceListeriosisMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutReceptors, TNF-Related Apoptosis-Inducing LigandSepsisTNF-Related Apoptosis-Inducing LigandReceptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing LigandTnfsf10 protein, mouse

Identifiers

PMID21788440
PMCPMC3159846
OpenAlexW2099206158

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.