Evidence map›Paper›PMID 19930040›Full record

ArticleImmunology2009

Toll-like receptor 4 signalling through MyD88 is essential to control Salmonella enterica serovar typhimurium infection, but not for the initiation of bacterial clearance.

Suzanne Talbot, Sabine Tötemeyer, Masahiro Yamamoto, Shizuo Akira, Katherine Hughes, David Gray, Tom Barr, Pietro Mastroeni, Duncan J Maskell, Clare E Bryant

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed, 64 citations in OpenAlex.

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  11. Type 1 interferon-dependent repression of NLRC4 and iPLA2 licenses down-regulation ofProceedings of the National Academy of Sciences of the United States of America · 2020
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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 3 institutions in 2 countries.

Suzanne TalbotDepartment of Veterinary Medicine, University of Cambridge, Cambridge, UK.
Sabine Tötemeyer
Masahiro Yamamoto
Shizuo Akira
Katherine Hughes
David Gray
Tom Barr
Pietro Mastroeni
Duncan J Maskell
Clare E Bryant
University of Cambridge · GBOsaka University · JPUniversity of Edinburgh · GB

Funding

Biotechnology and Biological Sciences Research Council BB/C005503/1Biotechnology and Biological Sciences Research Council BB/H003916/1
6 · The paper itself

Abstract

Toll-like receptor-4 (TLR4) is important in protection against lethal Salmonella enterica serovar Typhimurium (S. Typhimurium) infection. Control of the early stages of sublethal S. Typhimurium infection in mice depends on TLR4-dependent activation of macrophages and natural killer (NK) cells to drive an inflammatory response. TLR4 signals through the adapter proteins Mal/MyD88 and TRIF-related adaptor molecule (TRAM)/TIR-domain-containing adaptor-inducing interferon-b (TRIF). In the mouse typhoid model we showed that TLR4 and MyD88, but not Mal or TRIF, are essential for the control of exponential S. Typhimurium growth. TRIF(-/-) mice have a higher bacterial load in comparison with wild-type mice during a sublethal infection because TRIF is important for bacterial killing during the first day of systemic disease. Minimal pro-inflammatory responses were induced by S. Typhimurium infection of macrophages from TLR4(-/-), MyD88(-/-) and TRIF(-/-) mice in vitro. Pro-inflammatory responses from Mal(-/-) macrophages were similar to those from wild-type cells. The pro-inflammatory responses of TRIF(-/-) macrophages were partially restored by the addition of interferon-gamma (IFN-gamma), and TRIF(-/-) mice produced markedly enhanced IFN-gamma levels, in comparison to wild-type mice, probably explaining why bacterial growth can be controlled in these mice. TLR4(-/-), MyD88(-/-), TRIF(-/-) and Mal(-/-) mice all initiated clearance of S. Typhimurium, suggesting that TLR4 signalling is not important in driving bacterial clearance in comparison to its critical role in controlling early bacterial growth in mouse typhoid.

Indexed as

AnimalsCells, CulturedInterferon-gammaLiverMacrophage ActivationMacrophagesMiceMice, Inbred C57BLMyeloid Differentiation Factor 88Nitric OxideSalmonella InfectionsSalmonella typhimuriumSignal TransductionSpleenToll-Like Receptor 4Tumor Necrosis Factor-alphaInterferon-gammaMyd88 protein, mouseMyeloid Differentiation Factor 88Nitric OxideTlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID19930040
PMCPMC2792132
OpenAlexW1964104352

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.