Evidence map›Paper›PMID 11134301›Full record

ArticleJournal of virology2001

Inducible expression of inflammatory chemokines in respiratory syncytial virus-infected mice: role of MIP-1alpha in lung pathology.

H A Haeberle, W A Kuziel, H J Dieterich, A Casola, Z Gatalica, R P Garofalo

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
11.8field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 176 citations in OpenAlex.

  1. Article
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  4. Review
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  8. Article
  9. Chemokines and chemokine receptors during COVID-19 infection.Computational and structural biotechnology journal · 2021
    Review
  10. Review
  11. Disruption of the airway epithelial barrier in a murine model of respiratory syncytial virus infection.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. HumanWellcome open research · 2018
    Article
  18. Article
  19. Article
  20. Article

27 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 4 institutions in 2 countries.

H A HaeberleDepartments of Pediatrics, The University of Texas Medical Branch, Galveston, Texas, USA.
W A Kuziel
H J Dieterich
A Casola
Z Gatalica
R P Garofalo
Universitätsklinikum Tübingen · DEPediatrics and Genetics · USThe University of Texas at Austin · USThe University of Texas Medical Branch at Galveston · US

Funding

MUCOSAL IMMUNE RESPONSE TO RESPIRATORY SYNCYTIAL VIRUSR01AI015939 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI GAROFALO, ROBERTO P · 1985 to 1998
–
NIAID NIH HHS AI15939
6 · The paper itself

Abstract

Lower respiratory tract disease caused by respiratory syncytial virus (RSV) is characterized by profound airway mucosa inflammation, both in infants with naturally acquired infection and in experimentally inoculated animal models. Chemokines are central regulatory molecules in inflammatory, immune, and infectious processes of the lung. In this study, we demonstrate that intranasal infection of BALB/c mice with RSV A results in inducible expression of lung chemokines belonging to the CXC (MIP-2 and IP-10), CC (RANTES, eotaxin, MIP-1beta, MIP-1alpha, MCP-1, TCA-3) and C (lymphotactin) families. Chemokine mRNA expression occurred as early as 24 h following inoculation and persisted for at least 5 days in mice inoculated with the highest dose of virus (10(7) PFU). In general, levels of chemokine mRNA and protein were dependent on the dose of RSV inoculum and paralleled the intensity of lung cellular inflammation. Immunohisthochemical studies indicated that RSV-induced expression of MIP-1alpha, one of the most abundantly expressed chemokines, was primarily localized in epithelial cells of the alveoli and bronchioles, as well as in adjoining capillary endothelium. Genetically altered mice with a selective deletion of the MIP-1alpha gene (-/- mice) demonstrated a significant reduction in lung inflammation following RSV infection, compared to control littermates (+/+ mice). Despite the paucity of infiltrating cells, the peak RSV titer in the lung of -/- mice was not significantly different from that observed in +/+ mice. These results provide the first direct evidence that RSV infection may induce lung inflammation via the early production of inflammatory chemokines.

Indexed as

AnimalsChemokine CCL3Chemokine CCL4FemaleHumansImmunohistochemistryInflammationLungMacrophage Inflammatory ProteinsMiceMice, Inbred BALB CRespiratory Syncytial VirusesRespiratory Syncytial Virus InfectionsVirus ReplicationChemokine CCL3Chemokine CCL4Macrophage Inflammatory Proteins

Identifiers

PMID11134301
PMCPMC113984
OpenAlexW2045385097

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.