ArticleJournal of virology2011
Role of interleukin-1 and MyD88-dependent signaling in rhinovirus infection.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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.
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.
Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Polymorphism in the TLR Adaptors of the Toll Signalling Pathway for Use in Livestock Breeding for Health Traits.International journal of molecular sciences · 2026Review
- Pyroptosis in Respiratory Virus Infections: A Narrative Review of Mechanisms, Pathophysiology, and Potential Therapeutic Interventions.Microorganisms · 2025Review
- Interleukin-1β promotes human metapneumovirus replication via activating the cGAS-STING pathway.Virus research · 2024Review
- Immunotherapeutic implications on targeting the cytokines produced in rhinovirus-induced immunoreactions.Frontiers in allergy · 2024Review
- Unraveling the molecular crosstalk between Atherosclerosis and COVID-19 comorbidity.Computers in biology and medicine · 2021Article
- Disease Models: Lung Models for Testing Drugs Against Inflammation and Infection.Handbook of experimental pharmacology · 2021Article
- Mechanism of Rhinovirus Immunity and Asthma.Frontiers in immunology · 2021Review
- Inflammasome activation is required for human rhinovirus-induced airway inflammation in naive and allergen-sensitized mice.Mucosal immunology · 2019Article
- DUSP10 Negatively Regulates the Inflammatory Response to Rhinovirus through Interleukin-1β Signaling.Journal of virology · 2019Article
- Airway Epithelial Cells Generate Pro-inflammatory Tenascin-C and Small Extracellular Vesicles in Response to TLR3 Stimuli and Rhinovirus Infection.Frontiers in immunology · 2019Article
- Host Components Contributing to Respiratory Syncytial Virus Pathogenesis.Frontiers in immunology · 2019Review
- Targeting of the Nasal Mucosa by Japanese Encephalitis Virus for Non-Vector-Borne Transmission.Journal of virology · 2018Article
- The Anti-inflammatory Effect of Alpha-1 Antitrypsin in Rhinovirus-infected Human Airway Epithelial Cells.Journal of clinical & cellular immunology · 2016Article
- TLR2 Activation Limits Rhinovirus-Stimulated CXCL-10 by Attenuating IRAK-1-Dependent IL-33 Receptor Signaling in Human Bronchial Epithelial Cells.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Human rhinovirus-induced inflammatory responses are inhibited by phosphatidylserine containing liposomes.Mucosal immunology · 2016Article
- Chitosan-based mucosal adjuvants: Sunrise on the ocean.Vaccine · 2015Review
- Nasal lavage VEGF and TNF-α levels during a natural cold predict asthma exacerbations.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2014Article
- Ion flux in the lung: virus-induced inflammasome activation.Trends in microbiology · 2014Article
- Article
- Phosphoinositide-3 kinase inhibition modulates responses to rhinovirus by mechanisms that are predominantly independent of autophagy.PloS one · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Rhinoviral infection is an important trigger of acute inflammatory exacerbations in patients with underlying airway disease. We have previously established that interleukin-1β (IL-1β) is central in the communication between epithelial cells and monocytes during the initiation of inflammation. In this study we explored the roles of IL-1β and its signaling pathways in the responses of airway cells to rhinovirus-1B (RV-1B) and further determined how responses to RV-1B were modified in a model of bacterial coinfection. Our results revealed that IL-1β dramatically potentiated RV-1B-induced proinflammatory responses, and while monocytes did not directly amplify responses to RV-1B alone, they played an important role in the responses observed with our coinfection model. MyD88 is the essential signaling adapter for IL-1β and most Toll-like receptors. To examine the role of MyD88 in more detail, we created stable MyD88 knockdown epithelial cells using short hairpin RNA (shRNA) targeted to MyD88. We determined that IL-1β/MyD88 plays a role in regulating RV-1B replication and the inflammatory response to viral infection of airway cells. These results identify central roles for IL-1β and its signaling pathways in the production of CXCL8, a potent neutrophil chemoattractant, in viral infection. Thus, IL-1β is a viable target for controlling the neutrophilia that is often found in inflammatory airway disease and is exacerbated by viral infection of the airways.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.