Evidence map›Paper›PMID 20081068›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010

Anti-inflammatory effect of MUC1 during respiratory syncytial virus infection of lung epithelial cells in vitro.

Yusheng Li, Darrell L Dinwiddie, Kevin S Harrod, Yong Jiang, K Chul Kim

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Mucins and Respiratory Virus Infection.Annual review of virology · 2026
    Review
  4. Evolution ofInternational journal of molecular sciences · 2026
    Review
  5. Article
  6. MUC1 in the upper-lower airway inflammatory continuum: an endotype-centered perspective.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Mucus and Mucins: The Underappreciated Host Defence System.Frontiers in cellular and infection microbiology · 2022
    Review
  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

5 authors at 3 institutions in 2 countries.

Yusheng LiDepartment of Physiology and Lung Center, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.
Darrell L Dinwiddie
Kevin S Harrod
Yong Jiang
K Chul Kim
Lovelace Respiratory Research Institute · USSouthern Medical University · CNTemple University · US

Funding

SIGNALING MECHANISM OF MUC1 MUCINR01HL047125 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI KIM, KWANG CHUL · 1991 to 2015
$4.5M
Anti-inflammatory role of MUC1 mucinR01HL081825 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KIM, KWANG CHUL · 2006 to 2010
$2.2M
NHLBI NIH HHS R01 HL-47125NHLBI NIH HHS R01 HL-81825
6 · The paper itself

Abstract

MUC1 is a transmembrane glycoprotein expressed on the apical surface of airway epithelial cells and plays an anti-inflammatory role during airway bacterial infection. In this study, we determined whether the anti-inflammatory effect of MUC1 is also operative during the respiratory syncytial virus (RSV) infection. The lung epithelial cell line A549 was treated with RSV, and the production of TNFalpha and the levels of MUC1 protein were monitored temporally during the course of infection by ELISA and Western blot analysis. Small inhibitory RNA (siRNA) transfection was utilized to assess the role of MUC1 in regulating RSV-mediated inflammatory responses by lung epithelial cells. Our results revealed that: 1) following RSV infection, an increase in MUC1 level was preceded by an increase in TNFalpha production and completely inhibited by soluble TNF receptor (TNFR); and 2) knockdown of MUC1 using MUC1 siRNA resulted in a greater increase in TNFalpha level following RSV infection compared with control siRNA treatment. We conclude that the RSV-induced increase in the TNFalpha levels upregulates MUC1 through its interaction with TNFR, which in turn suppresses further increase in TNFalpha by RSV, thus forming a negative feedback loop in the control of RSV-induced inflammation. This is the first demonstration showing that MUC1 can suppress the virus-induced inflammatory responses.

Indexed as

AnimalsAnti-Inflammatory AgentsCell Line, TumorEpithelial CellsFeedback, PhysiologicalGene Expression RegulationGene Knockdown TechniquesHumansLungMiceMucin-1Receptors, Tumor Necrosis FactorRespiratory Syncytial VirusesRespiratory Syncytial Virus InfectionsRNA, MessengerSolubilityAnti-Inflammatory AgentsMucin-1Receptors, Tumor Necrosis FactorRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID20081068
PMCPMC2853342
OpenAlexW2165700760

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.