Evidence map›Paper›PMID 19139077›Full record

ArticleBlood2009

SHIP prevents lipopolysaccharide from triggering an antiviral response in mice.

Laura M Sly, Melisa J Hamilton, Etsushi Kuroda, Victor W Ho, Frann L Antignano, Stephanie L Omeis, Christina J van Netten-Thomas, Dana Wong, Hayley K Brugger, Olusegun Williams and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  11. Review
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  16. Article
  17. Inhibitor and activator: dual functions for SHIP in immunity and cancer.Annals of the New York Academy of Sciences · 2011
    Review
  18. IBD 2009: emerging research frontiers on the path to a cure.Canadian journal of gastroenterology = Journal canadien de gastroenterologie · 2010
    Article
  19. Article
  20. Article
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

15 authors at 3 institutions in 2 countries.

Laura M SlyTerry Fox Laboratory, British Columbia Cancer Research Centre, British Columbia Cancer Agency, Vancouver, BC, Canada.
Melisa J Hamilton
Etsushi Kuroda
Victor W Ho
Frann L Antignano
Stephanie L Omeis
Christina J van Netten-Thomas
Dana Wong
Hayley K Brugger
Olusegun Williams
Morris E Feldman
Benjamin T Houseman
Dorothea Fiedler
Kevan M Shokat
Gerald Krystal
BC Cancer Agency · CAUniversity of California, San Francisco · USHoward Hughes Medical Institute · US

Funding

Using chemical genetics to investigate mechanisms of anesthetic actionR01EB001987 · NIBIB · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHOKAT, KEVAN M. · 2003 to 2012
$2.9M
Howard Hughes Medical InstituteNIBIB NIH HHS 3R01EB0001987-12S1NIBIB NIH HHS R01 EB001987
6 · The paper itself

Abstract

Gram-negative bacterial infections, unlike viral infections, do not typically protect against subsequent viral infections. This is puzzling given that lipopolysaccharide (LPS) and double-stranded (ds) RNA both activate the TIR domain-containing adaptor-inducing interferon beta (TRIF) pathway and, thus, are both capable of eliciting an antiviral response by stimulating type I interferon (IFN) production. We demonstrate herein that SH2-containing inositol-5'-phosphatase (SHIP) protein levels are dramatically increased in murine macrophages via the MyD88-dependent pathway, by up-regulating autocrine-acting transforming growth factor-beta (TGFbeta). The increased SHIP then mediates, via inhibition of the phosphatidylinositol-3-kinase (PI3K) pathway, cytosine-phosphate-guanosine (CPG)- and LPS-induced tolerance and cross-tolerance and restrains IFN-beta production induced by a subsequent exposure to LPS or dsRNA. Intriguingly, we found, using isoform-specific PI3K inhibitors, that LPS- or cytosine-phosphate-guanosine-induced interleukin-6 (IL-6) is positively regulated by p110alpha, -gamma, and -delta but negatively regulated by p110beta. This may explain some of the controversy concerning the role of PI3K in Toll-like receptor-induced cytokine production. Consistent with our in vitro findings, SHIP(-/-) mice overproduce IFN-beta in response to LPS, and this leads to antiviral hypothermia. Thus, up-regulation of SHIP in response to Gram-negative bacterial infections probably explains the inability of such infections to protect against subsequent viral infections.

Indexed as

AnimalsCells, CulturedCpG IslandsGene Expression RegulationHypothermiaImmune ToleranceImmunity, InnateInositol Polyphosphate 5-PhosphatasesInterferon-betaLipopolysaccharidesMacrophagesMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88Phosphoric Monoester HydrolasesInositol Polyphosphate 5-PhosphatasesInterferon-betaLipopolysaccharidesMyd88 protein, mouseMyeloid Differentiation Factor 88Phosphoric Monoester HydrolasesRNA, Double-StrandedTransforming Growth Factor beta

Identifiers

PMID19139077
PMCPMC2662641
OpenAlexW2034988351

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.