ArticlemBio2018
Serum High-Mobility-Group Box 1 as a Biomarker and a Therapeutic Target during Respiratory Virus Infections.
Article in mBio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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
27 citing papers in PubMed, 45 citations in OpenAlex.
- Stem cell-based therapeutic strategies for liver aging.Liver research (Beijing, China) · 2025Review
- Enterovirus D68 infection in cotton rats results in systemic inflammation with detectable viremia associated with extracellular vesicle and neurologic disease.Scientific reports · 2025Article
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- Insight into the lncRNA-mRNA Co-Expression Profile and ceRNA Network in Lipopolysaccharide-Induced Acute Lung Injury.Current issues in molecular biology · 2023Article
- The role of HMGB1 in COVID-19-induced cytokine storm and its potential therapeutic targets: A review.Immunology · 2023Review
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- Graphene-Based Biosensors for Molecular Chronic Inflammatory Disease Biomarker Detection.Biosensors · 2022Review
- Acteoside attenuates RSV-induced lung injury by suppressing necroptosis and regulating metabolism.Frontiers in pharmacology · 2022Article
- Article
- TLRs in COVID-19: How they drive immunopathology and the rationale for modulation.Innate immunity · 2021Review
- Role of DAMPs in respiratory virus-induced acute respiratory distress syndrome-with a preliminary reference to SARS-CoV-2 pneumonia.Genes and immunity · 2021Review
- Complement Decay-Accelerating Factor is a modulator of influenza A virus lung immunopathology.PLoS pathogens · 2021Article
- Is Toll-like receptor 4 involved in the severity of COVID-19 pathology in patients with cardiometabolic comorbidities?Cytokine & growth factor reviews · 2021Review
- HMGB1, anti-HMGB1 antibodies, and ratio of HMGB1/anti-HMGB1 antibodies as diagnosis indicator in fever of unknown origin.Scientific reports · 2021Article
- Effect of aging on immunogenicity and efficacy of inactivated influenza vaccines in cotton ratsHuman vaccines & immunotherapeutics · 2021Article
- Gut Microbiota Dysbiosis Is a Crucial Player for the Poor Outcomes for COVID-19 in Elderly, Diabetic and Hypertensive Patients.Frontiers in medicine · 2021Review
- Targeting TLR4 Signaling to Blunt Viral-Mediated Acute Lung Injury.Frontiers in immunology · 2021Review
- The role of RAGE in host pathology and crosstalk between RAGE and TLR4 in innate immune signal transduction pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- Role of Damage-Associated Molecular Patterns in Light of Modern Environmental Research: A Tautological Approach.International journal of environmental research · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Host-derived "danger-associated molecular patterns" (DAMPs) contribute to innate immune responses and serve as markers of disease progression and severity for inflammatory and infectious diseases. There is accumulating evidence that generation of DAMPs such as oxidized phospholipids and high-mobility-group box 1 (HMGB1) during influenza virus infection leads to acute lung injury (ALI). Treatment of influenza virus-infected mice and cotton rats with the Toll-like receptor 4 (TLR4) antagonist Eritoran blocked DAMP accumulation and ameliorated influenza virus-induced ALI. However, changes in systemic HMGB1 kinetics during the course of influenza virus infection in animal models and humans have yet to establish an association of HMGB1 release with influenza virus infection. To this end, we used the cotton rat model that is permissive to nonadapted strains of influenza A and B viruses, respiratory syncytial virus (RSV), and human rhinoviruses (HRVs). Serum HMGB1 levels were measured by an enzyme-linked immunosorbent assay (ELISA) prior to infection until day 14 or 18 post-infection. Infection with either influenza A or B virus resulted in a robust increase in serum HMGB1 levels that decreased by days 14 to 18. Inoculation with the live attenuated vaccine FluMist resulted in HMGB1 levels that were significantly lower than those with infection with live influenza viruses. RSV and HRVs showed profiles of serum HMGB1 induction that were consistent with their replication and degree of lung pathology in cotton rats. We further showed that therapeutic treatment with Eritoran of cotton rats infected with influenza B virus significantly blunted serum HMGB1 levels and improved lung pathology, without inhibiting virus replication. These findings support the use of drugs that block HMGB1 to combat influenza virus-induced ALI.
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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.