ArticleVirology2013
Interleukin-1 receptor-associated kinase M (IRAK-M) promotes human rhinovirus infection in lung epithelial cells via the autophagic pathway.
Article in Virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- The Effect of a TLR3 Agonist on Airway Allergic Inflammation and Viral Infection in Immunoproteasome-Deficient Mice.Viruses · 2024Article
- The relationship between autophagy and respiratory viruses.Archives of microbiology · 2024Review
- The Role of the NRF2 Pathway in the Pathogenesis of Viral Respiratory Infections.Pathogens (Basel, Switzerland) · 2023Review
- Rhinovirus and Cell Death.Viruses · 2021Review
- A synthetic STING agonist inhibits the replication of human parainfluenza virus 3 and rhinovirus 16 through distinct mechanisms.Antiviral research · 2020Article
- Tollip Inhibits ST2 Signaling in Airway Epithelial Cells Exposed to Type 2 Cytokines and Rhinovirus.Journal of innate immunity · 2020Article
- Dynamically characterizing individual clinical change by the steady state of disease-associated pathway.BMC bioinformatics · 2019Article
- Interleukin 1 Receptor-Like 1 (IL1RL1) Promotes Airway Bacterial and Viral Infection and Inflammation.Infection and immunity · 2019Article
- IRAK-M Associates with Susceptibility to Adult-Onset Asthma and Promotes Chronic Airway Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Cellular and molecular mechanisms involved in the resolution of innate leukocyte inflammation.Journal of leukocyte biology · 2018Review
- Immunoproteasomes as a novel antiviral mechanism in rhinovirus-infected airways.Clinical science (London, England : 1979) · 2018Article
- Overproduction of growth differentiation factor 15 promotes human rhinovirus infection and virus-induced inflammation in the lung.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients.The Journal of allergy and clinical immunology · 2017Review
- A novel mouse model of conditional IRAK-M deficiency in myeloid cells: application in lung Pseudomonas aeruginosa infection.Innate immunity · 2017Article
- Effect of IRAK-M on Airway Inflammation Induced by Cigarette Smoking.Mediators of inflammation · 2017Article
- Airway gene expression of IL-1 pathway mediators predicts exacerbation risk in obstructive airway disease.International journal of chronic obstructive pulmonary disease · 2017Article
- Tollip SNP rs5743899 modulates human airway epithelial responses to rhinovirus infection.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2016Article
- The Anti-inflammatory Effect of Alpha-1 Antitrypsin in Rhinovirus-infected Human Airway Epithelial Cells.Journal of clinical & cellular immunology · 2016Article
- Cistrome-based Cooperation between Airway Epithelial Glucocorticoid Receptor and NF-κB Orchestrates Anti-inflammatory Effects.The Journal of biological chemistry · 2016Article
- Endothelial cell tolerance to lipopolysaccharide challenge is induced by monophosphoryl lipid A.Clinical science (London, England : 1979) · 2016Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Human rhinovirus (HRV) is the most common viral etiology in acute exacerbations of asthma. However, the exact mechanisms underlying HRV infection in allergic airways are poorly understood. IL-13 increases interleukin-1 receptor associated kinase M (IRAK-M) and subsequently inhibits airway innate immunity against bacteria. However, the role of IRAK-M in lung HRV infection remains unclear. Here, we provide the first evidence that IRAK-M over-expression promotes lung epithelial HRV-16 replication and autophagy, but inhibits HRV-16-induced IFN-β and IFN-λ1 expression. Inhibiting autophagy reduces HRV-16 replication. Exogenous IFN-β and IFN-λ1 inhibit autophagy and HRV-16 replication. Our data indicate the enhancing effect of IRAK-M on epithelial HRV-16 infection, which is partly through the autophagic pathway. Impaired anti-viral interferon production may serve as a direct or an indirect (e.g., autophagy) mechanism of enhanced HRV-16 infection by IRAK-M over-expression. Targeting autophagic pathway or administrating anti-viral interferons may prevent or attenuate viral (e.g., HRV-16) infections in allergic airways.
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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.