Evidence map›Paper›PMID 20090954›Full record

ArticlePloS one2010

Dynamic innate immune responses of human bronchial epithelial cells to severe acute respiratory syndrome-associated coronavirus infection.

Tomoki Yoshikawa, Terence E Hill, Naoko Yoshikawa, Vsevolod L Popov, Cristi L Galindo, Harold R Garner, C J Peters, Chien-Te Kent Tseng

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 3 pooled it
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

133 citing papers in PubMed, 3 syntheses or guidelines pooled it, 209 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Review
  7. Extra gene coding capacity of SARS-CoV-2 provides a virus engineering platform for in vitro and in vivo applications.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  8. Article
  9. Exploring the Role ofACS infectious diseases · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

73 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

8 authors at 2 institutions in 1 country.

Tomoki YoshikawaDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, United States of America.
Terence E Hill
Naoko Yoshikawa
Vsevolod L Popov
Cristi L Galindo
Harold R Garner
C J Peters
Chien-Te Kent Tseng
The University of Texas Medical Branch at Galveston · USSouthwestern Medical Center · US

Funding

WRCE Nonhuman Primate CoreU54AI057156 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI WALKER, DAVID H · 2003 to 2013
$102.6M
U.S. Based Collaboration in Emerging Viral DiseasesN01AI25489 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI TESH, ROBERT B · 2007 to 2010
$4.3M
Inflammatory Response and SARS Pathogenesis: An in vitro ModelR21AI072201 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI TSENG, CHIEN-TE K · 2007 to 2009
$633k
U.S. Based Collaboration in Emerging Viral and Prion Diseases-26625489N01AI025489 · NIAID · University of Texas Medical Branch · 2004 to 2004
–
NIAID NIH HHS N01 AI025489NIAID NIH HHS N01 AI25489NIAID NIH HHS N01 AI3009NIAID NIH HHS R21 AI072201NIAID NIH HHS R21AI072201NIAID NIH HHS U54 AI057156
6 · The paper itself

Abstract

Human lung epithelial cells are likely among the first targets to encounter invading severe acute respiratory syndrome-associated coronavirus (SARS-CoV). Not only can these cells support the growth of SARS-CoV infection, but they are also capable of secreting inflammatory cytokines to initiate and, eventually, aggravate host innate inflammatory responses, causing detrimental immune-mediated pathology within the lungs. Thus, a comprehensive evaluation of the complex epithelial signaling to SARS-CoV is crucial for paving the way to better understand SARS pathogenesis. Based on microarray-based functional genomics, we report here the global gene response of 2B4 cells, a cloned bronchial epithelial cell line derived from Calu-3 cells. Specifically, we found a temporal and spatial activation of nuclear factor (NF)kappaB, activator protein (AP)-1, and interferon regulatory factor (IRF)-3/7 in infected 2B4 cells at 12-, 24-, and 48-hrs post infection (p.i.), resulting in the activation of many antiviral genes, including interferon (IFN)-beta, -lambdas, inflammatory mediators, and many IFN-stimulated genes (ISGs). We also showed, for the first time, that IFN-beta and IFN-lambdas were capable of exerting previously unrecognized, non-redundant, and complementary abilities to limit SARS-CoV replication, even though their expression could not be detected in infected 2B4 bronchial epithelial cells until 48 hrs p.i. Collectively, our results highlight the mechanics of the sequential events of antiviral signaling pathway/s triggered by SARS-CoV in bronchial epithelial cells and identify novel cellular targets for future studies, aiming at advancing strategies against SARS.

Indexed as

Immunity, InnateBronchiCells, CulturedEpithelial CellsGene ExpressionHumansInterferon Regulatory Factor-3Interferon Regulatory Factor-7NF-kappa BSevere Acute Respiratory SyndromeSevere acute respiratory syndrome-related coronavirusVirus ReplicationInterferon Regulatory Factor-3Interferon Regulatory Factor-7NF-kappa B

Identifiers

PMID20090954
PMCPMC2806919
OpenAlexW2058008662

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.