Evidence map›Paper›PMID 28375519›Full record

ArticleThe Journal of infectious diseases2017

Impact of Type I and III Interferons on Respiratory Superinfections Due to Multidrug-Resistant Pathogens.

Dane Parker

Abstract read
In one paragraph

Article in The Journal of infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Review
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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

1 author.

Dane ParkerDepartment of Pediatrics, Columbia University, New York.

Funding

Role of interferons in Staphylococcus aureus upper respiratory tract infectionR56HL125653 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PARKER, DANE · 2015 to 2015
$384k
NHLBI NIH HHS R56 HL125653
6 · The paper itself

Abstract

The increased morbidity and mortality associated with bacterial pneumonias that are acquired following influenza infection are well appreciated by clinicians. One of the major components of the immune response to influenza is the induction of the types I and III interferon cascades, which encompasses the activation of over 300 genes. The immunological consequences of IFN activation, while important for viral clearance, modify the host proinflammatory responses through effects on the inflammasome, Th17 signaling and recruitment of phagocytic cells. IFN signaling affects both susceptibility to subsequent Streptococcus pneumoniae and Staphylococcus aureus infection as well as the intensity of the immune responses associated with pulmonary damage. Appreciation for the effects of IFN activation on anti-bacterial pulmonary defense mechanisms should help to inform therapeutic strategies in an ICU setting.

Indexed as

Anti-Bacterial AgentsDrug Resistance, Multiple, BacterialHost-Pathogen InteractionsHumansInflammasomesInterferonsMicrobiotaMorbidityPneumococcal InfectionsPneumonia, BacterialRespiratory SystemRespiratory Tract DiseasesStaphylococcal InfectionsStaphylococcus aureusStreptococcus pneumoniaeSuperinfectionAnti-Bacterial AgentsInflammasomesInterferonsinfluenzapneumoniaStaphylococcus aureusStreptococcus pneumoniaesuperinfectiontype III interferontype I interferon

Identifiers

PMID28375519
PMCPMC5853883

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.