Evidence map›Paper›PMID 29893825›Full record

ArticleFEMS microbiology reviews2018

Staphylococcus aureus modulation of innate immune responses through Toll-like (TLR), (NOD)-like (NLR) and C-type lectin (CLR) receptors.

Fatemeh Askarian, Theresa Wagner, Mona Johannessen, Victor Nizet

Open access · bronzeAbstract read
In one paragraph

Article in FEMS microbiology reviews, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing 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

61 citing papers in PubMed, 102 citations in OpenAlex.

  1. Staphylococcus aureus-vascular endothelium interactions: Mechanisms and therapeutic opportunities.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026
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  9. Overcoming Immune Evasion inACS infectious diseases · 2025
    Review
  10. Review
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  16. Review
  17. DNA PAMPs as Molecular Tools for the cGAS-STING Signaling Pathways.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  18. Article
  19. Review
  20. Article

1 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

4 authors at 2 institutions in 2 countries.

Fatemeh AskarianResearch Group of Host Microbe Interaction, Faculty of Health Sciences, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.
Theresa WagnerResearch Group of Host Microbe Interaction, Faculty of Health Sciences, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.
Mona JohannessenResearch Group of Host Microbe Interaction, Faculty of Health Sciences, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.
Victor NizetDivision of Host-Microbe Systems & Therapeutics, Department of Pediatrics, UC San Diego, La Jolla, CA 92093, USA.
UiT The Arctic University of Norway · NOUniversity of California, San Diego · US

Funding

Systems Biology Approach to Redefine Susceptibility Testing and Treatment of MDR Pathogens in the Context of Host ImmunityU01AI124316 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PALSSON, BERNHARD O · 2016 to 2020
$10.2M
Glycoprotein Remodeling in the Vasculopathy and Coagulopathy of SepsisR01HL125352 · NHLBI · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI MARTH, JAMEY, NIZET, VICTOR · 2014 to 2018
$3.6M
NHLBI NIH HHS R01 HL125352NIAID NIH HHS U01 AI124316
6 · The paper itself

Abstract

Early recognition of pathogens by the innate immune system is crucial for bacterial clearance. Many pattern recognition receptors (PRRs) such as Toll-like (TLRs) and (NOD)-like (NLRs) receptors have been implicated in initial sensing of bacterial components. The intracellular signaling cascades triggered by these receptors result in transcriptional upregulation of inflammatory pathways. Although this step is crucial for bacterial elimination, it is also associated with the potential for substantial immunopathology, which underscores the need for tight control of inflammatory responses. The leading human bacterial pathogen Staphylococcus aureus expresses over 100 virulence factors that exert numerous effects upon host cells. In this manner, the pathogen seeks to avoid host recognition or perturb PRR-induced innate immune responses to allow optimal survival in the host. These immune system interactions may result in enhanced bacterial proliferation but also provoke systemic cytokine responses associated with sepsis. This review summarizes recent findings on the various mechanisms applied by S. aureus to modulate or interfere with inflammatory responses through PRRs. Detailed understanding of these complex interactions can provide new insights toward future immune-stimulatory therapeutics against infection or immunomodulatory therapeutics to suppress or correct dysregulated inflammation.

Indexed as

Immunity, InnateLectins, C-TypeNLR ProteinsStaphylococcus aureusToll-Like ReceptorsLectins, C-TypeNLR ProteinsToll-Like Receptors

Identifiers

PMID29893825
PMCPMC6098222
OpenAlexW2805071569

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.