Evidence map›Paper›PMID 26516184›Full record

ArticleJournal of leukocyte biology2016

The inflammasome NLRP3 plays a protective role against a viral immunopathological lesion.

Fernanda Gimenez, Siddheshvar Bhela, Pranay Dogra, Lorena Harvey, Siva Karthik Varanasi, Ujjaldeep Jaggi, Barry T Rouse

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Alternative cGAS signaling promotes herpes simplex encephalitis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  5. Meeting the Challenge of Controlling Viral Immunopathology.International journal of molecular sciences · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Fernanda GimenezDepartment of Biomedical and Diagnostic Sciences, University of Tennessee, Knoxville, Tennessee, USA;
Siddheshvar BhelaDepartment of Biomedical and Diagnostic Sciences, University of Tennessee, Knoxville, Tennessee, USA;
Pranay DograDepartment of Microbiology, University of Tennessee, Knoxville, Tennessee, USA; and.
Lorena HarveyDepartment of Biomedical and Diagnostic Sciences, University of Tennessee, Knoxville, Tennessee, USA;
Siva Karthik VaranasiDepartment of Genome Science and Technology, University of Tennessee, Knoxville, Tennessee, USA.
Ujjaldeep JaggiDepartment of Biomedical and Diagnostic Sciences, University of Tennessee, Knoxville, Tennessee, USA;
Barry T RouseDepartment of Biomedical and Diagnostic Sciences, University of Tennessee, Knoxville, Tennessee, USA; btr@utk.edu.
University of Tennessee at Knoxville · US

Funding

Mechanisms of Herpetic KeratitisR01EY005093 · NEI · UNIVERSITY OF TENNESSEE KNOXVILLE · PI ROUSE, BARRY T. · 1985 to 2020
$7.8M
T regulatory Cells in HSV Immunity and ImmunopathologyR01AI063365 · NIAID · UNIVERSITY OF TENNESSEE KNOXVILLE · PI ROUSE, BARRY T. · 2006 to 2015
$3.5M
NEI NIH HHS R01 EY005093NIAID NIH HHS R01 AI063365
6 · The paper itself

Abstract

Herpes simplex 1 infection of the eye can cause blindness with lesions in the corneal stroma largely attributable to inflammatory events that include components of both adaptive and innate immunity. Several innate immune responses are triggered by herpes simplex 1, but it is unclear how such innate events relate to the subsequent development of stromal keratitis. In this study, we compared the outcome of herpes simplex 1 ocular infection in mice unable to express NLRP3 because of gene knockout (NLRP3(-/-)) to that of wild-type mice. The NLRP3(-/-) mice developed more-severe and earlier stromal keratitis lesions and had higher angiogenesis scores than did infected wild-type animals. In addition, NLRP3(-/-) mice generated an increased early immune response with heightened chemokines and cytokines, including interleukin-1β and interleukin-18, and elevated recruitment of neutrophils. Increased numbers of CD4(+) T cells were seen at later stages of the disease in NLRP3(-/-) animals. Reduction in neutrophils prevented early onset of the disease in NLRP3(-/-) animals and lowered levels of bioactive interleukin-1β but did not lower bioactive interleukin-18. In conclusion, our results indicate that NLRP3 has a regulatory and beneficial role in herpetic stromal keratitis pathogenesis.

Indexed as

AnimalsCorneaFemaleHerpesvirus 1, HumanInflammasomesInflammation MediatorsInterleukin-18Interleukin-1betaKeratitisLymph NodesMice, Inbred C57BLNeutrophilsNLR Family, Pyrin Domain-Containing 3 ProteinProtective AgentsTh17 CellsTh1 CellsInflammasomesInflammation MediatorsInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseProtective AgentsHSVinflammationstromal keratitis

Identifiers

PMID26516184
PMCPMC4831481
OpenAlexW2248741584

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.