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Lower respiratory tract delivery, airway clearance, and preclinical efficacy of inhaled GM-CSF in a postinfluenza pneumococcal pneumonia model. | LitMetric

AI Article Synopsis

  • Inhaled granulocyte/macrophage colony-stimulating factor (GM-CSF) shows potential for treating pneumonia caused by viruses and bacteria, but a suitable mouse model hasn't been created yet.
  • Researchers aimed to develop this model to test the effects of aerosolized GM-CSF on survival during influenza A virus infection and its impact on subsequent bacterial infections.
  • The study found that while inhaled GM-CSF significantly improved survival against secondary bacterial challenges, it did not reduce bacterial growth in the lungs, suggesting its protective effects may enhance lung resistance to infections rather than lower bacterial levels directly.*

Article Abstract

Inhaled granulocyte/macrophage colony-stimulating factor (GM-CSF) shows promise as a therapeutic to treat viral and bacterial pneumonia, but no mouse model of inhaled GM-CSF has been described. We sought to ) develop a mouse model of aerosolized recombinant mouse GM-CSF administration and ) investigate the protection conferred by inhaled GM-CSF during influenza A virus (IAV) infection against secondary bacterial infection with pneumococcus. To assess lower respiratory tract delivery of aerosolized therapeutics, mice were exposed to aerosolized fluorescein (FITC)-labeled dextran noninvasively via an aerosolization tower or invasively using a rodent ventilator. The efficiency of delivery to the lower respiratory tracts of mice was 0.01% noninvasively compared with 0.3% invasively. The airway pharmacokinetics of inhaled GM-CSF fit a two-compartment model with a terminal phase half-life of 1.3 h. To test if lower respiratory tract levels were sufficient for biological effect, mice were infected intranasally with IAV, treated with aerosolized recombinant mouse GM-CSF, and then secondarily infected with . Inhaled GM-CSF conferred a significant survival benefit to mice against secondary challenge with ( < 0.05). Inhaled GM-CSF did not reduce airway or lung parenchymal bacterial growth but significantly reduced the incidence of bacteremia ( < 0.01). However, GM-CSF overexpression during influenza virus infection did not affect lung epithelial permeability to FITC-dextran ingress into the bloodstream. Therefore, the mechanism of protection conferred by inhaled GM-CSF appears to be locally mediated improved lung antibacterial resistance to systemic bacteremia during IAV infection.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7191485PMC
http://dx.doi.org/10.1152/ajplung.00296.2019DOI Listing

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