ArticleCellular & molecular immunology2015
Soluble interleukin-6 receptor is elevated during influenza A virus infection and mediates the IL-6 and IL-32 inflammatory cytokine burst.
Article in Cellular & molecular immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Association of SARS-CoV-2 infection with long-lasting increase in circulating IL-32 levels.Frontiers in immunology · 2026Observational
- Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025Review
- LDC000067, a CDK9 inhibitor, unveils promising results in suppressing influenza virus infectionsAntimicrobial agents and chemotherapy · 2025Article
- Innate immune role of IL-6 in influenza a virus pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- IL-32-driven neutrophil activation in preeclampsia.Cellular & molecular immunology · 2023Article
- Subaqueous free-standing 3D cell culture system for ultrafast cell compaction, mechano-inductive immune control, and improving therapeutic angiogenesis.Bioengineering & translational medicine · 2023Article
- Anti-inflammatory actions of Pentosan polysulfate sodium in a mouse model of influenza virus A/PR8/34-induced pulmonary inflammation.Frontiers in immunology · 2023Article
- IL-6/STAT3 Signaling Axis Enhances and Prolongs Pdcd1 Expression in Murine CD8 T Cells.ImmunoHorizons · 2022Article
- Immune system-related soluble mediators and COVID-19: basic mechanisms and clinical perspectives.Cell communication and signaling : CCS · 2022Review
- Cytokine profiles in the detection of severe lung involvement in hospitalized patients with COVID-19: The IL-8/IL-32 axis.Cytokine · 2022Article
- Herbo-mineral formulation, Divya-Swasari-Vati averts SARS-CoV-2 pseudovirus entry into human alveolar epithelial cells by interfering with spike protein-ACE 2 interaction and IL-6/TNF-α /NF-κB signaling.Frontiers in pharmacology · 2022Article
- Thymus Gland: A Double Edge Sword for Coronaviruses.Vaccines · 2021Review
- Liver injury in COVID-19 and IL-6 trans-signaling-induced endotheliopathy.Journal of hepatology · 2021Article
- The Mechanism behind Influenza Virus Cytokine Storm.Viruses · 2021Review
- Placenta-derived IL-32β activates neutrophils to promote preeclampsia development.Cellular & molecular immunology · 2021Article
- Comorbidities and inflammation associated with ovarian cancer and its influence on SARS-CoV-2 infection.Journal of ovarian research · 2021Review
- Modulation of the Tissue Expression Pattern of Zebrafish CRP-Like Molecules Suggests a Relevant Antiviral Role in Fish Skin.Biology · 2021Article
- Coronil, a Tri-Herbal Formulation, Attenuates Spike-Protein-Mediated SARS-CoV-2 Viral Entry into Human Alveolar Epithelial Cells and Pro-Inflammatory Cytokines Production by Inhibiting Spike Protein-ACE-2 Interaction.Journal of inflammation research · 2021Article
- Potential Molecular Mechanisms and Remdesivir Treatment for Acute Respiratory Syndrome Corona Virus 2 Infection/COVID 19 Through RNA Sequencing and Bioinformatics Analysis.Bioinformatics and biology insights · 2021Article
- SARS-CoV-2 spike protein promotes IL-6 trans-signaling by activation of angiotensin II receptor signaling in epithelial cells.PLoS pathogens · 2020Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV) infection is a major worldwide public health problem. However, the factors involved in mediating the inflammatory response to this infection and their relationships remain poorly understood. Here, we show that IAV infection stimulates the expression of the soluble IL-6 receptor (sIL-6R), a multifunctional protein involved in IL-6 signaling. Interestingly, sIL-6R expression upregulated the levels of its own ligand, IL-6 and those of the pro-inflammatory cytokine IL-32. shRNA-mediated knockdown of sIL-6R suppressed IL-6 and IL-32, indicating that this regulation is dependent on sIL-6R during IAV infection. Furthermore, our results demonstrate that IL-32 participates in a negative feedback loop that inhibits sIL-6R while upregulating IL-6 expression during IAV infection. Therefore, we show that sIL-6R is a critical cellular factor involved in the acute inflammatory response to viral infection.
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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.