ArticlePloS one2019
Enhanced IL-1β production is mediated by a TLR2-MYD88-NLRP3 signaling axis during coinfection with influenza A virus and Streptococcus pneumoniae.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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
22 citing papers in PubMed, 35 citations in OpenAlex.
- Hypoxia-inducible factor-1α exacerbates immune injury induced by influenza A virus and Streptococcus pneumoniae coinfection.BMC infectious diseases · 2025Article
- Post-influenza bacterial infection: mechanisms of pathogenesis and advances in therapeutic strategies.Frontiers in microbiology · 2025Review
- Characteristics of adults with influenza A virus pneumonia and co-infections identified by mNGS in Jilin, China during 2024-2025.Frontiers in cellular and infection microbiology · 2025Article
- Parkinson's disease models and death signaling: what do we know until now?Frontiers in neuroanatomy · 2024Review
- Article
- The Influenza-Induced Pulmonary Inflammatory Exudate in Susceptible Tpl2-Deficient Mice Is Dictated by Type I IFN Signaling.Inflammation · 2023Article
- Vitamin D and the Ability to Produce 1,25(OH)Nutrients · 2022Article
- Bacterial and Viral Co-Infection in the Intestine: Competition Scenario and Their Effect on Host Immunity.International journal of molecular sciences · 2022Review
- Pathogenesis of Respiratory Viral and Fungal Coinfections.Clinical microbiology reviews · 2022Review
- Altered Signal Transduction in the Immune Response to Influenza Virus andInternational journal of molecular sciences · 2021Review
- Suppressive Effect of Two Cucurbitane-Type Triterpenoids fromMolecules (Basel, Switzerland) · 2021Article
- Virus-Induced Changes of the Respiratory Tract Environment Promote Secondary Infections WithFrontiers in cellular and infection microbiology · 2021Review
- The Role of Innate Immunity in Pulmonary Infections.BioMed research international · 2021Review
- IL 33 Correlates With COVID-19 Severity, Radiographic and Clinical Finding.Frontiers in medicine · 2021Article
- Imperfect storm: is interleukin-33 the Achilles heel of COVID-19?The Lancet. Rheumatology · 2020Review
- Scutellarin ameliorates pulmonary fibrosis through inhibiting NF-κB/NLRP3-mediated epithelial-mesenchymal transition and inflammation.Cell death & disease · 2020Article
- SARS-CoV-2 Infection and Cardioncology: From Cardiometabolic Risk Factors to Outcomes in Cancer Patients.Cancers · 2020Review
- NLRP3 as Putative Marker of Ipilimumab-Induced Cardiotoxicity in the Presence of Hyperglycemia in Estrogen-Responsive and Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2020Article
- Programmed Cell Death in the Evolutionary Race against Bacterial Virulence Factors.Cold Spring Harbor perspectives in biology · 2020Review
- Respiratory Barrier as a Safeguard and Regulator of Defense Against Influenza A Virus andFrontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Viral-bacterial coinfections, such as with influenza A virus and Streptococcus pneumoniae (S.p.), are known to cause severe pneumonia. It is well known that the host response has an important role in disease. Interleukin-1β (IL-1β) is an important immune signaling cytokine responsible for inflammation and has been previously shown to contribute to disease severity in numerous infections. Other studies in mice indicate that IL-1β levels are dramatically elevated during IAV-S.p. coinfection. However, the regulation of IL-1β during coinfection is unknown. Here, we report the NLRP3 inflammasome is the major inflammasome regulating IL-1β activation during coinfection. Furthermore, elevated IL-1β mRNA expression is due to enhanced TLR2-MYD88 signaling, which increases the amount of pro-IL-1β substrate for the inflammasome to process. Finally, NLRP3 and high IL-1β levels were associated with increased bacterial load in the brain. Our results show the NLRP3 inflammasome is not protective during IAV-S.p. coinfection.
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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.