ArticleFrontiers in immunology2022
Gelsolin Attenuates Neonatal Hyperoxia-Induced Inflammatory Responses to Rhinovirus Infection and Preserves Alveolarization.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The trial behind it
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- A Phase 1, Single-Center, Randomized, Double-Blind, Placebo-Controlled, Multiple-Dose Escalation Study for the Evaluation of the Safety, Tolerability, and Pharmacokinetics of Recombinant Human Plasma Gelsolin (rhu-pGSN) Following Intravenous Administration to Healthy Volunteers.Clinical pharmacology in drug development · 2026Trial
- Lactoferrin blocks orthopoxvirus entry via heparan sulphate and regulates host antiviral pathways.Emerging microbes & infections · 2026Article
- Age-dependent immune responses and resident cell dynamics in young mice following pneumonia.iScience · 2026Article
- Interpretable machine learning uncovers epithelial transcriptional rewiring and a role for Gelsolin in COPD.JCI insight · 2024Article
- Gelsolin regulates intestinal stem cell regeneration and Th17 cellular function.Cell communication and signaling : CCS · 2024Article
- Systemic mechanisms of necrotic cell debris clearance.Cell death & disease · 2024Review
- IL-17a-producing γδT cells and NKG2D signaling mediate bacterial endotoxin-induced neonatal lung injury: implications for bronchopulmonary dysplasia.Frontiers in immunology · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Prematurity and bronchopulmonary dysplasia (BPD) increase the risk of asthma later in life. Supplemental oxygen therapy is a risk factor for chronic respiratory symptoms in infants with BPD. Hyperoxia induces cell injury and release of damage-associated molecular patterns (DAMPs). Cytoskeletal filamentous actin (F-actin) is a DAMP which binds Clec9a, a C-type lectin selectively expressed on CD103+ dendritic cells (DCs). Co-stimulation of Clec9a and TLR3 induces maximal proinflammatory responses. We have shown that neonatal hyperoxia (a model of BPD) increases lung IL-12+Clec9a+CD103+ DCs, pro-inflammatory responses and airway hyperreactivity following rhinovirus (RV) infection. CD103+ DCs and Clec9a are required for these responses. Hyperoxia increases F-actin levels in bronchoalveolar lavage fluid (BALF). We hypothesized that the F-actin severing protein gelsolin attenuates neonatal hyperoxia-induced Clec9a+CD103+ DC-dependent pro-inflammatory responses to RV and preserves alveolarization. We exposed neonatal mice to hyperoxia and treated them with gelsolin intranasally. Subsequently we inoculated the mice with RV intranasally. Alternatively, we inoculated normoxic neonatal mice with BALF from hyperoxia-exposed mice (hyperoxic BALF), RV and gelsolin. We analyzed lung gene expression two days after RV infection. For
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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.