ArticleMolecular therapy : the journal of the American Society of Gene Therapy2023
Preventing occludin tight-junction disruption via inhibition of microRNA-193b-5p attenuates viral load and influenza-induced lung injury.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 26 citations in OpenAlex.
- Disease landscape-guided design of neutrophil-specific reporters for early and accurate pneumonia detection in vivo and in urine.Science advances · 2026Article
- Influenza B virus suppression of Chromosome Y-linked genes increases pulmonary virus replication and disease severity in male mice.Research square · 2026Article
- Comparative progress on the mechanisms of airway mucosal injury induced by different pathogens: SARS-CoV-2, influenza A virus, and Mycoplasma pneumoniae.Frontiers in cellular and infection microbiology · 2026Review
- Non-coding RNAs: master regulators in the battle between host antiviral defense and viral replication.Frontiers in immunology · 2026Review
- Occludin-mediated barrier dysfunction and its role in cardiovascular and cerebrovascular pathogenesis.Frontiers in cardiovascular medicine · 2026Review
- MacrophageAutophagy · 2025Article
- Gut microbiota modulates CNS barrier function in murine model for multiple sclerosis.Fluids and barriers of the CNS · 2025Article
- Newcastle disease virus promotes spreading infection through vimentin-dependent tight junction injury mediated by MLC/p-MLC activation.PLoS pathogens · 2025Article
- Age Matters: Key Contributors to Interferon Toxicity in Infants During Influenza Virus Infection.Viruses · 2025Review
- Influenza virus-induced type I interferons disrupt alveolar epithelial repair and tight junction integrity in the developing lung.Mucosal immunology · 2025Article
- Screening out microRNAs and Their Molecular Pathways with a Potential Role in the Regulation of Parvovirus B19 Infection Through In Silico Analysis.International journal of molecular sciences · 2025Article
- Positive Regulation of Cellular Proteins by Influenza Virus for Productive Infection.International journal of molecular sciences · 2025Review
- INTESTINAL EPITHELIAL-SPECIFIC OCCLUDIN DELETION WORSENS GUT PERMEABILITY AND SURVIVAL FOLLOWING SEPSIS.Shock (Augusta, Ga.) · 2025Article
- Transcriptional analysis reveals the suppression of RAD51 and disruption of the homologous recombination pathway during PEDV infection in IPEC-J2 cells.Virology journal · 2024Article
- The Molecular Basis of Asthma Exacerbations Triggered by Viral Infections: The Role of Specific miRNAs.International journal of molecular sciences · 2024Review
- Rujin Jiedu decoction protects against influenza virus infection by modulating gut microbiota.Heliyon · 2024Article
- Tiny Guides, Big Impact: Focus on the Opportunities and Challenges of miR-Based Treatments for ARDS.International journal of molecular sciences · 2024Review
- Occludin: a gatekeeper of brain Infection by HIV-1.Fluids and barriers of the CNS · 2023Review
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Authors and funding
24 authors at 8 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Virus-induced lung injury is associated with loss of pulmonary epithelial-endothelial tight junction integrity. While the alveolar-capillary membrane may be an indirect target of injury, viruses may interact directly and/or indirectly with miRs to augment their replication potential and evade the host antiviral defense system. Here, we expose how the influenza virus (H1N1) capitalizes on host-derived interferon-induced, microRNA (miR)-193b-5p to target occludin and compromise antiviral defenses. Lung biopsies from patients infected with H1N1 revealed increased miR-193b-5p levels, marked reduction in occludin protein, and disruption of the alveolar-capillary barrier. In C57BL/6 mice, the expression of miR-193b-5p increased, and occludin decreased, 5-6 days post-infection with influenza (PR8). Inhibition of miR-193b-5p in primary human bronchial, pulmonary microvascular, and nasal epithelial cells enhanced antiviral responses. miR-193b-deficient mice were resistant to PR8. Knockdown of occludin, both in vitro and in vivo, and overexpression of miR-193b-5p reconstituted susceptibility to viral infection. miR-193b-5p inhibitor mitigated loss of occludin, improved viral clearance, reduced lung edema, and augmented survival in infected mice. Our results elucidate how the innate immune system may be exploited by the influenza virus and how strategies that prevent loss of occludin and preserve tight junction function may limit susceptibility to virus-induced lung injury.
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