Evidence map›Paper›PMID 29226710›Full record

ReviewFuture microbiology2018

Group A Streptococcus encounters with host macrophages.

J Andrés Valderrama, Victor Nizet

Open access · greenAbstract readReview
In one paragraph

Review in Future microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Increasing Rate of FatalMicroorganisms · 2024
    Article
  3. [Research progress on the mechanism of -lactam resistance in group AZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024
    Review
  4. Article
  5. Article
  6. Streptococcal peptides and their roles in host-microbe interactions.Frontiers in cellular and infection microbiology · 2023
    Review
  7. Article
  8. AmBio · 2021
    Article
  9. Article
  10. Evaluation of IL-17D in Host Immunity to Group AJournal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  11. Review
  12. Article
  13. Article
  14. Nicotinamide Increases Intracellular NADFrontiers in microbiology · 2020
    Article
  15. Article
  16. Functional and Proteomic Analysis ofFrontiers in microbiology · 2019
    Article
  17. Group AMicrobiology spectrum · 2019
    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

2 authors at 1 institution in 1 country.

J Andrés ValderramaDepartment of Pediatrics, University of California, San Diego, La Jolla, CA 92093, USA.
Victor NizetDepartment of Pediatrics, University of California, San Diego, La Jolla, CA 92093, USA.
University of California, San Diego · US

Funding

GAS Switch from Colonizing Bacterium to Invasive PathogenR01AI077780 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI NIZET, VICTOR · 2008 to 2019
$3.8M
Mechanisms of the M protein in group A Streptococcus virulenceR01AI096837 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GHOSH, PARTHO, NIZET, VICTOR · 2011 to 2015
$2.7M
Mechanisms of the M protein in group A Streptococcus virulenceR56AI096837 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GHOSH, PARTHO, NIZET, VICTOR · 2018 to 2018
$540k
NIAID NIH HHS R01 AI077780NIAID NIH HHS R01 AI096837NIAID NIH HHS R56 AI096837
6 · The paper itself

Abstract

Group A Streptococcus (GAS) is a leading human bacterial pathogen with diverse clinical manifestations. Macrophages constitute a critical first line of host defense against GAS infection, using numerous surface and intracellular receptors such as Toll-like receptors and inflammasomes for pathogen recognition and activation of inflammatory signaling pathways. Depending on the intensity of the GAS infection, activation of these signaling cascades may provide a beneficial early alarm for effective immune clearance, or conversely, may cause hyperinflammation and tissue injury during severe invasive infection. Although traditionally considered an extracellular pathogen, GAS can invade and replicate within macrophages using specific molecular mechanisms to resist phagolysosomal and xenophagic killing. Unraveling GAS-macrophage encounters may reveal new treatment options for this leading agent of infection-associated mortality. [Formula: see text].

Indexed as

AnimalsHumansInflammasomesMacrophagesStreptococcal InfectionsStreptococcus pyogenesInflammasomesGroup A Streptococcus (GAS)IL-1β signalingintracellular survivalmacrophageNLRP3 inflammasomephagocytosisToll-like receptorsxenophagy

Identifiers

PMID29226710
PMCPMC5771463
OpenAlexW2772316791

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.