Evidence map›Paper›PMID 21646453›Full record

ArticleInfection and immunity2011

The Toll-like receptor 4 agonist monophosphoryl lipid a augments innate host resistance to systemic bacterial infection.

Christopher D Romero, Tushar K Varma, Jason B Hobbs, Aimee Reyes, Brandon Driver, Edward R Sherwood

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

75 citing papers in PubMed, 109 citations in OpenAlex.

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  20. Therapeutic applications of toll-like receptors (TLRs) agonists in AML.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review

15 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Christopher D RomeroDepartment of Anesthesiology, University of Texas Medical Branch, Galveston, TX 77555-0591, USA.
Tushar K Varma
Jason B Hobbs
Aimee Reyes
Brandon Driver
Edward R Sherwood
Shriners Hospitals for Children - Galveston · USThe University of Texas Medical Branch at Galveston · US

Funding

Resistance of Beta 2 Microglobulin Null Mice to SepsisR01GM066885 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SHERWOOD, EDWARD R · 2003 to 2016
$4.4M
Augmentation of Innate Anti-Microbial Immunity by TLR4 AgonistsR01GM104306 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ENKHBAATAR, PERENLEI, SHERWOOD, EDWARD R · 2013 to 2016
$1.2M
Mechanisms of Monophosporyl Lipid A Immuno-Modulation in Septic ShockF31AI080159 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI ROMERO, CHRISTOPHER-DAVID MICHAEL · 2009 to 2010
$58k
NIAID NIH HHS F31 AI080159NIGMS NIH HHS R01 GM066885NIGMS NIH HHS R01 GM104306NIGMS NIH HHS R01 GM66885
6 · The paper itself

Abstract

Monophosphoryl lipid A (MPLA) is a Toll-like receptor 4 (TLR4) agonist that is currently used as a vaccine adjuvant in humans. In this study, we evaluated the effect of MPLA treatment on the innate immune response to systemic bacterial infections in mice. Mice treated with MPLA after burn injury showed improved survival and less local and systemic dissemination of bacteria in a model of Pseudomonas aeruginosa burn wound infection. Prophylactic treatment with MPLA significantly enhanced bacterial clearance at the site of infection and reduced systemic dissemination of bacteria despite causing attenuation of proinflammatory cytokine production during acute intra-abdominal infection caused by cecal ligation and puncture. Administration of MPLA at 1 h after CLP also improved bacterial clearance but did not alter cytokine production. MPLA treatment increased the numbers of granulocytes, double-positive myeloid cells, and macrophages at sites of infection and increased the percentage and total numbers of myeloid cells mediating phagocytosis of bacteria. Depletion of Ly6G(+) neutrophils, but not macrophages, eliminated the ability of MPLA treatment to improve bacterial clearance. The immunomodulatory effects of MPLA were absent in TLR4-deficient mice. In conclusion, these studies show that MPLA treatment significantly augments the innate immune response to bacterial infection by enhancing bacterial clearance despite the attenuation of proinflammatory cytokine production. The enhanced bacterial clearance is mediated, in part, by increased numbers of myeloid cells with effective phagocytic functions at sites of infection and is TLR4 dependent.

Indexed as

Immunity, InnateAnimalsBurnsCytokinesFemaleLipid ALymphocyte CountMacrophagesMaleMiceMice, Inbred C3HMice, Inbred C57BLNeutrophilsPseudomonas aeruginosaPseudomonas InfectionsSignal TransductionCytokinesLipid Amonophosphoryl lipid ATlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID21646453
PMCPMC3165493
OpenAlexW2103236172

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.