Evidence map›Paper›PMID 34282358›Full record

ReviewFrontiers in immunology2021

Targeting TLR4 Signaling to Blunt Viral-Mediated Acute Lung Injury.

Kari Ann Shirey, Jorge C G Blanco, Stefanie N Vogel

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Alternative splicing of toll-like receptor pathway mRNAs in lung immune cells from patients with ARDS.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. A narrative review of chemokine receptors CXCR1 and CXCR2 and their role in acute respiratory distress syndrome.European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  19. Review
  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

3 authors at 2 institutions in 1 country.

Kari Ann ShireyDepartment of Microbiology and Immunology, School of Medicine, University of Maryland, Baltimore, MD, United States.
Jorge C G BlancoSigmovir Biosystems, Inc., Rockville, MD, United States.
Stefanie N VogelDepartment of Microbiology and Immunology, School of Medicine, University of Maryland, Baltimore, MD, United States.
University of Maryland, Baltimore · USSigmovir Biosystems (United States) · US

Funding

Eritoran (E5564), a TLR4 antagonist, as a novel therapeutic for influenzaR01AI104541 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI BLANCO, JORGE C, VOGEL, STEFANIE N. · 2013 to 2016
$3.4M
Targeting TLR Signaling Pathways to Blunt Pathogen-mediated Acute Lung InjuryR01AI125215 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI BLANCO, JORGE C, VOGEL, STEFANIE N. · 2017 to 2021
$2.7M
Macrophage differentiation and disease outcome in influenza infectionR01AI123371 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI VOGEL, STEFANIE N. · 2017 to 2021
$2.7M
RSV-induced M2 macrophage differentiation: role of TLR4/PPARg/RXR signaling axis (80)R21AI163543 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI BLANCO, JORGE C, VOGEL, STEFANIE N. · 2021 to 2022
$432k
Neuroendocrine control of TLR4-dependent inflammation in influenzaR21AI159507 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI SHIREY, KARI ANN · 2021 to 2022
$411k
NIAID NIH HHS R01 AI104541NIAID NIH HHS R01 AI123371NIAID NIH HHS R01 AI125215NIAID NIH HHS R21 AI159507NIAID NIH HHS R21 AI163543
6 · The paper itself

Abstract

Respiratory viral infections have been a long-standing global burden ranging from seasonal recurrences to the unexpected pandemics. The yearly hospitalizations from seasonal viruses such as influenza can fluctuate greatly depending on the circulating strain(s) and the congruency with the predicted strains used for the yearly vaccine formulation, which often are not predicted accurately. While antiviral agents are available against influenza, efficacy is limited due to a temporal disconnect between the time of infection and symptom development and viral resistance. Uncontrolled, influenza infections can lead to a severe inflammatory response initiated by pathogen-associated molecular patterns (PAMPs) or host-derived danger-associated molecular patterns (DAMPs) that ultimately signal through pattern recognition receptors (PRRs). Overall, these pathogen-host interactions result in a local cytokine storm leading to acute lung injury (ALI) or the more severe acute respiratory distress syndrome (ARDS) with concomitant systemic involvement and more severe, life threatening consequences. In addition to traditional antiviral treatments, blocking the host's innate immune response may provide a more viable approach to combat these infectious pathogens. The SARS-CoV-2 pandemic illustrates a critical need for novel treatments to counteract the ALI and ARDS that has caused the deaths of millions worldwide. This review will examine how antagonizing TLR4 signaling has been effective experimentally in ameliorating ALI and lethal infection in challenge models triggered not only by influenza, but also by other ALI-inducing viruses.

Indexed as

Acute Lung InjuryAntiviral AgentsCOVID-19Cytokine Release SyndromeHumansLungPandemicsSARS-CoV-2Signal TransductionToll-Like Receptor 4Antiviral AgentsToll-Like Receptor 4ALIHMGB1influenzaTLR4viruses

Identifiers

PMID34282358
PMCPMC8285366
OpenAlexW3184859363

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.