Evidence map›Paper›PMID 25213347›Full record

ArticleInnate immunity2015

MyD88-mediated TLR signaling protects against acute rotavirus infection while inflammasome cytokines direct Ab response.

Robin Uchiyama, Benoit Chassaing, Benyue Zhang, Andrew T Gewirtz

Open access · greenAbstract read
In one paragraph

Article in Innate immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  5. Article
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  8. Review
  9. Article
  10. Article
  11. Rotavirus infection.Nature reviews. Disease primers · 2017
    Review
  12. Article
  13. Article
  14. Review
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

4 authors at 2 institutions in 1 country.

Robin UchiyamaCenter for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA Immunology and Molecular Pathogenesis Graduate Program, Emory University, Atlanta, GA, USA.
Benoit ChassaingCenter for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA.
Benyue ZhangCenter for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA.
Andrew T GewirtzCenter for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA Immunology and Molecular Pathogenesis Graduate Program, Emory University, Atlanta, GA, USA agewirtz@gsu.edu.
Georgia State University · USEmory University · US

Funding

Pathophysiology of TLR5KO ColitisR01DK083890 · NIDDK · GEORGIA STATE UNIVERSITY · PI GEWIRTZ, ANDREW T · 2010 to 2023
$5.0M
Flagellin-Induced Antiviral ActivityR21AI107943 · NIAID · GEORGIA STATE UNIVERSITY · PI GEWIRTZ, ANDREW T · 2014 to 2015
$407k
NIAID NIH HHS AI107943NIAID NIH HHS R21 AI107943NIDDK NIH HHS DK083890NIDDK NIH HHS R01 DK083890
6 · The paper itself

Abstract

Rotavirus (RV) infects small intestinal epithelial cells, inducing severe diarrhea in children, resulting in over 500,000 deaths annually. Relatively little is known about how innate immunity contains acute infection and drives adaptive immune responses that afford complete clearance of RV and protection against future infection. Hence, we examined the consequence of the absence of MyD88, known to be central to innate immunity, in a mouse model of RV infection. The absence of MyD88, but not combined blockade of IL-1β and IL-18 signaling, resulted in greater infectivity, as reflected by levels of RV in feces, intestinal lysates and viremia. Such increased RV levels correlated with an increase in incidence and duration of diarrhea. Loss of MyD88 also impaired humoral immunity to RV. Specifically, MyD88 knockout generated less RV-specific IgA and exhibited profoundly reduced RV-specific IgG2c/IgG1 ratios suggesting that MyD88 signaling drives RV-induced Th1 responses. A study of MyD88 bone marrow chimeras indicated that MyD88-dependent control of acute RV infection was mediated by both hemopoietic and non-hemopoietic cells, while generation of RV-specific humoral immunity was driven by MyD88 signaling in hemopoietic cells, which reflected the loss of IL-1β and IL-18 expression by these cells. Thus, TLR signaling and inflammasome cytokines drive innate and adaptive immunity to RV.

Indexed as

Acute DiseaseAnimalsAntibody FormationCells, CulturedCytokinesDisease Models, AnimalHumansImmunity, InnateInflammasomesInterleukin-18Interleukin-1betaMaleMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88CytokinesInflammasomesInterleukin-18Interleukin-1betaMyeloid Differentiation Factor 88Toll-Like ReceptorsantibodyinflammasomeMyD88RotavirusToll-like receptors

Identifiers

PMID25213347
PMCPMC7534410
OpenAlexW1987224020

What OpenQuestion holds

Textmetadata
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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.