ArticleBMC immunology2009
The toll-Like receptor adaptor TRIF contributes to otitis media pathogenesis and recovery.
Article in BMC immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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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
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Dysregulation of immune response in otitis media.Expert reviews in molecular medicine · 2021Pooled it
- Pattern recognition receptor signaling in otitis media: immune crosstalk and pathogenic mechanisms.Frontiers in immunology · 2026Review
- Toll-Like Receptors: Expression and Roles in Otitis Media.International journal of molecular sciences · 2021Review
- Panel 2- recent advance in otitis media bioinformatics.International journal of pediatric otorhinolaryngology · 2020Review
- A2ML1 and otitis media: novel variants, differential expression, and relevant pathways.Human mutation · 2019Article
- Lack of the hyaluronan receptor CD44 affects the course of bacterial otitis media and reduces leukocyte recruitment to the middle ear.BMC immunology · 2019Article
- Toll-Like Receptor 3-TRIF Pathway Activation byInfection and immunity · 2019Article
- Current Understanding of Host Genetics of Otitis Media.Frontiers in genetics · 2019Review
- Review
- Innate Immunity: Orchestrating Inflammation and Resolution of Otitis Media.Current allergy and asthma reports · 2016Review
- The inflammasome adaptor ASC contributes to multiple innate immune processes in the resolution of otitis media.Innate immunity · 2015Article
- NOD-Like Receptor Signaling in Cholesteatoma.BioMed research international · 2015Article
- What have we learned from murine models of otitis media?Current allergy and asthma reports · 2013Review
- A protective Hsp70-TLR4 pathway in lethal oxidant lung injury.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Panel 4: Recent advances in otitis media in molecular biology, biochemistry, genetics, and animal models.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2013Review
- Panel 5: Microbiology and immunology panel.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2013Review
- Ecrg4 attenuates the inflammatory proliferative response of mucosal epithelial cells to infection.PloS one · 2013Article
- Type I interferon response to extracellular bacteria in the airway epithelium.Trends in immunology · 2011Review
- Clinical approaches for understanding the expression levels of pattern recognition receptors in otitis media with effusion.Clinical and experimental otorhinolaryngology · 2011Article
- Exome sequencing identifies a missense mutation in Isl1 associated with low penetrance otitis media in dearisch mice.Genome biology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundToll-like receptor (TLR) signalling is crucial for innate immune responses to infection. The involvement of TLRs in otitis media (OM), the most prevalent childhood disease in developed countries, has been implicated by studies in middle ear cell lines, by association studies of TLR-related gene polymorphisms, and by altered OM in mice bearing mutations in TLR genes. Activated TLRs signal via two alternative intracellular signaling molecules with differing effects; MyD88 (Myeloid differentiation primary response gene 88) inducing primarily interleukin expression and TRIF (Tir-domain-containing adaptor inducing interferon beta) mediating type I interferon (IFN) expression. We tested the hypothesis that TRIF and type I IFN signaling play a role in OM, using a murine model of OM induced by non-typeable Haemophilus influenzae (NTHi). The ME inflammatory response to NTHi was examined in wild-type (WT) and TRIF-/- mice by qPCR, gene microarray, histopathology and bacterial culture.
resultsExpression of TRIF mRNA was only modesty enhanced during OM, but both type I IFN signalling genes and type I IFN-inducible genes were significantly up-regulated in WT mice. TRIF-deficient mice showed reduced but more persistent mucosal hyperplasia and less leukocyte infiltration into the ME in response to NTHi infection than did WT animals. Viable bacteria could be cultured from MEs of TRIF-/- mice for much longer in the course of disease than was the case for middle ears of WT mice.
conclusionOur results demonstrate that activation of TRIF/type I IFN responses is important in both the pathogenesis and resolution of NTHi-induced OM.
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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.