Evidence map›Paper›PMID 23989337›Full record

ReviewShock (Augusta, Ga.)2013

The immunobiology of toll-like receptor 4 agonists: from endotoxin tolerance to immunoadjuvants.

Julia K Bohannon, Antonio Hernandez, Perenlei Enkhbaatar, William L Adams, Edward R Sherwood

Abstract readReview
In one paragraph

Review in Shock (Augusta, Ga.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

85 citing papers in PubMed, 133 citations in OpenAlex.

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25 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

5 authors at 2 institutions in 1 country.

Julia K Bohannon*Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee; †Department of Anesthesiology, The University of Texas Medical Branch, Galveston, Texas; and ‡School of Medicine, The University of Tennessee Health Science Center, Memphis; and §Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.
Antonio Hernandez
Perenlei Enkhbaatar
William L Adams
Edward R Sherwood
Vanderbilt University Medical Center · 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
NIGMS NIH HHS R01 GM066885NIGMS NIH HHS R01 GM104306NIGMS NIH HHS R01 GM66885
6 · The paper itself

Abstract

Lipopolysaccharide (LPS, endotoxin) is a structural component of the gram-negative outer membrane. The lipid A moiety of LPS binds to the LPS receptor complex expressed by leukocytes, endothelial cells, and parenchymal cells and is the primary component of gram-negative bacteria that is recognized by the immune system. Activation of the LPS receptor complex by native lipid A induces robust cytokine production, leukocyte activation, and inflammation, which is beneficial for clearing bacterial infections at the local level but can cause severe systemic inflammation and shock at higher challenge doses. Interestingly, prior exposure to LPS renders the host resistant to shock caused by subsequent LPS challenge, a phenomenon known as endotoxin tolerance. Treatment with lipid A has also been shown to augment the host response to infection and to serve as a potent vaccine adjuvant. However, the adverse effects associated with the pronounced inflammatory response limit the use of native lipid A as a clinical immunomodulator. More recently, analogs of lipid A have been developed that possess attenuated proinflammatory activity but retain attractive immunomodulatory properties. The lipid A analog monophosphoryl lipid A exhibits approximately 1/1,000th of the toxicity of native lipid A but retains potent immunoadjuvant activity. As such, monophosphoryl lipid A is currently used as an adjuvant in several human vaccine preparations. Because of the potency of lipid A analogs as immunoadjuvants, numerous laboratories are actively working to identify and develop new lipid A mimetics and to optimize their efficacy and safety. Based on those characteristics, lipid A analogs represent an attractive family of immunomodulators.

Indexed as

Adjuvants, ImmunologicAnimalsBacterial InfectionsCytokinesEndotoxinsHumansImmune ToleranceImmunity, InnateLipopolysaccharidesToll-Like Receptor 4Adjuvants, ImmunologicCytokinesEndotoxinsLipopolysaccharidesTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID23989337
PMCPMC3919163
OpenAlexW2027328983

What OpenQuestion holds

Textmetadata
LicenceTDM
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.