Evidence map›Paper›PMID 21881124›Full record

ArticleThe Journal of infectious diseases2011

Lowering the threshold of lung innate immune cell activation alters susceptibility to secondary bacterial superinfection.

John Goulding, Alexandra Godlee, Seema Vekaria, Markus Hilty, Robert Snelgrove, Tracy Hussell

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.3field-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

65 citing papers in PubMed, 111 citations in OpenAlex.

  1. Review
  2. Viruses in bronchiectasis.ERJ open research · 2025
    Review
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  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Monocytes and Macrophages in COVID-19.Frontiers in immunology · 2021
    Review
  15. Article
  16. Review
  17. Changes in physiology and immune system during pregnancy and coronavirus infection: A review.European journal of obstetrics, gynecology, and reproductive biology · 2020
    Review
  18. Article
  19. COVID-19 and islet transplantation: Different twins.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020
    Review
  20. Article

5 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

6 authors at 1 institution in 1 country.

John GouldingLeukocyte Biology Section, Imperial College London, National Heart and Lung Institute, United Kingdom.
Alexandra Godlee
Seema Vekaria
Markus Hilty
Robert Snelgrove
Tracy Hussell
Imperial College London · GB

Funding

New Strategies to Prevent Death from InfluenzaU01AI070232 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SMITH, KENDALL A · 2006 to 2010
$6.1M
Medical Research Council G0802752Medical Research Council P171/03/C1/048NIAID NIH HHS 1 U01 AI070232-01Wellcome Trust 082727/Z/07/Z
6 · The paper itself

Abstract

backgroundPrevious studies have shown that the interaction of CD200R, a myeloid inhibitory receptor, with its ligand, CD200, is critical in the control of innate immune activation in the lung. METHODS AND

resultsUsing a mouse model of bacterial superinfection following influenza, we show that an absence of CD200R (a negative regulator highly expressed by macrophages and dendritic cells), restricts commensal and exogenous bacterial invasiveness and completely prevents the mortality observed in wild-type mice. This benefit is due to a heightened innate immune response to influenza virus in cd200r knockout mice that limits immune pathogenesis and viral load. In wild-type mice, apoptotic cells expressing CD200 that we believe contribute to the suppressed innate immune response to bacteria dominate during the resolution phase of influenza-induced inflammation. We also show for the first time the presence of a variety of previously unidentified bacterial species in the lower airways that are significantly adjusted by influenza virus infection and may contribute to the pathophysiology of disease.

conclusionsThe interaction of CD200 with CD200R therefore contributes to the hyporesponsive innate immune state following influenza virus infection that predisposes to secondary bacterial infection, a phenomenon that has the potential for immune modulation.

Indexed as

AnimalsAntigens, CDBronchoalveolar Lavage FluidFemaleImmunity, InnateInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H3N2 SubtypeInterleukin-1LungMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutModels, AnimalOrthomyxoviridae InfectionsPneumonia, PneumococcalAntigens, CDantigens, CD200CD200 receptor, mouseInterleukin-1Membrane GlycoproteinsTumor Necrosis Factor-alpha

Identifiers

PMID21881124
PMCPMC3164429
OpenAlexW2167233568

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.