Evidence map›Paper›PMID 28328242›Full record

ArticleAmerican journal of respiratory cell and molecular biology2017

Human Airway Epithelial Cells Direct Significant Rhinovirus Replication in Monocytic Cells by Enhancing ICAM1 Expression.

Xu Zhou, Lingxiang Zhu, Rosa Lizarraga, Yin Chen

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Up-Regulated Vitamin D Receptor byPharmaceuticals (Basel, Switzerland) · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Extracellular Vesicles in Viral Infections: Two Sides of the Same Coin?Frontiers in cellular and infection microbiology · 2020
    Review
  12. Rhinovirus and Innate Immune Function of Airway Epithelium.Frontiers in cellular and infection microbiology · 2020
    Review
  13. Rhinovirus Attributes that Contribute to Asthma Development.Immunology and allergy clinics of North America · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Xu ZhouDepartment of Pharmacology and Toxicology, School of Pharmacy, University of Arizona, Tucson, Arizona.
Lingxiang ZhuDepartment of Pharmacology and Toxicology, School of Pharmacy, University of Arizona, Tucson, Arizona.
Rosa LizarragaDepartment of Pharmacology and Toxicology, School of Pharmacy, University of Arizona, Tucson, Arizona.
Yin ChenDepartment of Pharmacology and Toxicology, School of Pharmacy, University of Arizona, Tucson, Arizona.
University of Arizona · US

Funding

Regulation of MUC19 by Th2 cytokine in airway epitheliumR01AI061695 · NIAID · UNIVERSITY OF ARIZONA · PI CHEN, YIN · 2007 to 2011
$1.9M
TLR3, TICAM1 and human rhinovirus infectionR21AI113526 · NIAID · UNIVERSITY OF ARIZONA · PI CHEN, YIN · 2014 to 2015
$417k
NIAID NIH HHS R01 AI061695NIAID NIH HHS R21 AI113526
6 · The paper itself

Abstract

Human rhinovirus (RV) is the major cause of common cold, and it also plays a significant role in asthma and asthma exacerbation. The airway epithelium is the primary site of RV infection and production. In contrast, monocytic cells (e.g., monocytes and macrophages) are believed to be nonpermissive for RV replication. Instead, RV has been shown to modulate inflammatory gene expressions in these cells via a replication-independent mechanism. In the study presented here, replication of RV16 (a major-group RV) was found to be significantly enhanced in monocytes when it was cocultivated with airway epithelial cells. This effect appeared to be mediated by secretory components from epithelial cells, which stimulated RV16 replication and significantly elevated the expression of a number of proinflammatory cytokines. The lack of such an effect on RV1A, a minor-group RV that enters the cell by a different receptor, suggests that intercellular adhesion molecule 1 (ICAM1), the receptor for major-group RVs, may be involved. Indeed, conditioned media from epithelial cells significantly increased ICAM1 expression in monocytes. Consistently, ICAM1 overexpression and ICAM1 knockdown enhanced and blocked RV production, respectively, confirming the role of ICAM1 in this process. Thus, this is the first report demonstrating that airway epithelial cells direct significant RV16 replication in monocytic cells via an ICAM1-dependent mechanism. This finding will open a new avenue for the study of RV infection in airway disease and its exacerbation.

Indexed as

Virus ReplicationAlveolar Epithelial CellsBronchiCell LineCoculture TechniquesCulture Media, ConditionedCytokinesDNA, ComplementaryGene Knockdown TechniquesHumansIntercellular Adhesion Molecule-1MonocytesPrimary Cell CultureReceptors, VirusRhinovirusRNA InterferenceCulture Media, ConditionedCytokinesDNA, ComplementaryICAM1 protein, humanIntercellular Adhesion Molecule-1Receptors, VirusRNA, MessengerRNA, Small InterferingairwayepitheliumICAM1rhinovirus

Identifiers

PMID28328242
PMCPMC5576581
OpenAlexW2603113790

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.