Evidence map›Paper›PMID 18714046›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Inhalation of Staphylococcus aureus enterotoxin A induces IFN-gamma and CD8 T cell-dependent airway and interstitial lung pathology in mice.

Guruprasaadh Muralimohan, Robert J Rossi, Linda A Guernsey, Roger S Thrall, Anthony T Vella

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. A Study on the Epidemiological-Molecular Role ofAntibiotics (Basel, Switzerland) · 2023
    Article
  2. Article
  3. IFN-American journal of respiratory cell and molecular biology · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Therapeutic blockade of CD54 attenuates pulmonary barrier damage in T cell-induced acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Presensitizing with a Toll-like receptor 3 ligand impairs CD8 T-cell effector differentiation and IL-33 responsiveness.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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

5 authors at 1 institution in 1 country.

Guruprasaadh MuralimohanDepartment of Immunology, University of Connecticut Health Center, Farmington, CT 06032, USA.
Robert J Rossi
Linda A Guernsey
Roger S Thrall
Anthony T Vella
UConn Health · US

Funding

Sustained adaptive immunity in the mucosaP01AI056172 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI VELLA, ANTHONY T · 2003 to 2017
$22.3M
PROINFLAMMATORY CYTOKINES BLOCK T CELL DEATH IN VIVOR01AI042858 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI VELLA, ANTHONY T · 1999 to 2016
$4.9M
Understanding the Mechanism of 4-1BB ConstimulatiuonR01AI052108 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI VELLA, ANTHONY T · 2003 to 2007
$1.4M
Understanding the mechanism of 4-1BB costimulationR21AI052108 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI VELLA, ANTHONY T. · 2002 to 2002
$326k
NIAID NIH HHS AI 142858NIAID NIH HHS AI 52108NIAID NIH HHS P01 AI056172NIAID NIH HHS R01 AI042858NIAID NIH HHS R01 AI052108NIAID NIH HHS R21 AI052108
6 · The paper itself

Abstract

Staphylococcus aureus, a primary source of bacterial superantigen (SAg), is known to colonize the human respiratory tract and has been implicated in airway inflammation. Studies have documented a role for SAgs in respiratory disorders, such as nasal polyps, chronic obstructive pulmonary disease, chronic rhinosinusitis, and asthma. However, cellular and molecular mediators involved in SAg-mediated pulmonary disease have not been clearly identified. In this study, we investigated the effect of intranasal staphylococcal enterotoxin A (SEA) exposure on murine lung. The pathological features in the lung resulting from SEA exposure had characteristics of both obstructive and restrictive pulmonary disorders. There was also an increase in bronchoalveolar lavage protein concentration and cellularity following SEA challenge. Massive CD8(+)Vbeta3(+) T cell accumulation observed in the lung was dependent on CD4 T cell help, both for recruitment and for IFN-gamma synthesis. The primary source of IFN-gamma synthesis was CD8 T cells, and depletion of these cells abrogated disease. IFN-gamma deficiency also prevented SEA-mediated disease, and this was by enhancing early recruitment of neutrophils as detected in the bronchoalveolar lavage. Thus, IFN-gamma appeared to selectively aid the recruitment of T cells to the lungs while preventing the neutrophil accumulation. Therefore, our results show that IFN-gamma-producing CD8 T cells mediated pulmonary alveolitis and inflammation, which were dependent upon CD4 T cells for their recruitment to the lung.

Indexed as

AnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesChemotaxis, LeukocyteEnterotoxinsInhalationInterferon-gammaLungLung DiseasesMiceNeutrophilsenterotoxin A, StaphylococcalEnterotoxinsInterferon-gamma

Identifiers

PMID18714046
PMCPMC2576742
OpenAlexW1596043305

What OpenQuestion holds

Textmetadata
LicenceTDM
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.