Evidence map›Paper›PMID 19786304›Full record

ArticleMolecular immunology2009

Role of alveolar epithelial early growth response-1 (Egr-1) in CD8+ T cell-mediated lung injury.

Chilakamarti V Ramana, Guang-Shing Cheng, Aseem Kumar, Hyung-Joo Kwon, Richard I Enelow

Abstract read
In one paragraph

Article in Molecular immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Impact of e-cigarette aerosol on primary human alveolar epithelial type 2 cells.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  2. Article
  3. Review
  4. EndogenousInternational journal of molecular sciences · 2019
    Article
  5. Egr-1 deficiency protects from renal inflammation and fibrosis.Journal of molecular medicine (Berlin, Germany) · 2016
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Immunopathogenesis of 2009 pandemic influenza.Enfermedades infecciosas y microbiologia clinica · 2012
    Review
  12. Review
  13. 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

5 authors at 4 institutions in 3 countries.

Chilakamarti V RamanaDepartment of Medicine, Dartmouth Medical School, Lebanon, NH 03756, USA. ramana.v.chilakamarti@dartmouth.edu
Guang-Shing Cheng
Aseem Kumar
Hyung-Joo Kwon
Richard I Enelow
Dartmouth College · USHallym University · KRLaurentian University · CAYale University · US

Funding

VASCULAR LEUKOCYTES: BASIC IMMUNOBIOLOGY AND FUNCTIONAL PLASTICITYP20RR016437 · NCRR · DARTMOUTH COLLEGE · PI GREEN, WILLIAM R · 2001 to 2010
$24.3M
Training Translational Lung Biology and PathobiologyT32HL007778 · NHLBI · YALE UNIVERSITY · PI Erica L Herzog, NAFTALI KAMINSKI · 1994 to 2026
$14.4M
TNF Processing in Pulmonary ImmunopathologyR01AI069360 · NIAID · DARTMOUTH COLLEGE · PI ENELOW, RICHARD I · 2007 to 2011
$1.8M
NCRR NIH HHS P20 RR016437NCRR NIH HHS P20 RR16437NHLBI NIH HHS T32HL007778NIAID NIH HHS R01 AI069360NIAID NIH HHS R01AI069360
6 · The paper itself

Abstract

Influenza infection of the distal airways results in severe lung injury, a considerable portion of which is immunopathologic and attributable to the host responses. We have used a mouse model to specifically investigate the role of antiviral CD8(+) T cells in this injury, and have found that the critical effector molecule is TNF-alpha expressed by the T cells upon antigen recognition. Interestingly, the immunopathology which ensues is characterized by significant accumulation of host inflammatory cells, recruited by chemokines expressed by the target alveolar epithelial cells. In this study we analyzed the mechanisms involved in the induction of epithelial chemokine expression triggered by antigen-specific CD8(+) T cell recognition, and demonstrate that the early growth response-1 (Egr-1) transcription factor is rapidly induced in epithelial cells, both in vitro and ex vivo, and that this is a critical regulator of a host of inflammatory chemokines. Genetic deficiency of Egr-1 significantly abrogates both the chemokine expression and the immunopathologic injury associated with T cell recognition, and it directly regulates transcriptional activity of a model CXC chemokine, MIP-2. We further demonstrate that Egr-1 induction is triggered by TNF-alpha-dependent ERK activation, and inhibition of this pathway ablates Egr-1 expression. These findings suggest that Egr-1 may represent an important target in mitigating the immunopathology of severe influenza infection.

Indexed as

Adoptive TransferAnimalsCD8-Positive T-LymphocytesChemokine CXCL2ChemokinesEarly Growth Response Protein 1Enzyme ActivationEpithelial CellsExtracellular Signal-Regulated MAP KinasesGene Expression ProfilingLung DiseasesMiceNF-kappa BPromoter Regions, GeneticProtein BindingPulmonary AlveoliChemokine CXCL2ChemokinesEarly Growth Response Protein 1Extracellular Signal-Regulated MAP KinasesNF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID19786304
PMCPMC2787734
OpenAlexW2113953901

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.