AI Article Synopsis

  • Viral-induced lower respiratory tract infections (LRTI), especially from RSV, significantly impact young children's health, leading to long-lasting respiratory issues.
  • This study used a mouse model to explore how exposure to high oxygen levels (hyperoxia) during a severe RSV infection affects long-term lung function and structure.
  • Results showed that hyperoxia led to temporary growth arrest and increased airway resistance without affecting lung structure, suggesting that high oxygen exposure during viral LRTI can worsen future lung health.

Article Abstract

Viral-induced lower respiratory tract infection (LRTI), mainly by respiratory syncytial virus (RSV), causes a major health burden among young children and has been associated with long-term respiratory dysfunction. Children with severe viral LRTI are frequently treated with oxygen therapy, hypothetically posing an additional risk factor for pulmonary sequelae. The main goal of this study was to determine the effect of concurrent hyperoxia exposure during the acute phase of viral LRTI on long-term pulmonary outcome. As an experimental model for severe RSV LRTI in infants, C57Bl/6J mice received an intranasal inoculation with the pneumonia virus of mice J3666 strain at post-natal day 7, and were subsequently exposed to hyperoxia (85% O) or normoxia (21% O) from post-natal day 10 to 17 during the acute phase of disease. Long-term outcomes, including lung function and structural development, were assessed 3 weeks post-inoculation at post-natal day 28. Compared to normoxic conditions, hyperoxia exposure in PVM-inoculated mice induced a transient growth arrest without subsequent catchup growth, as well as a long-term increase in airway resistance. This hyperoxia-induced pulmonary dysfunction was not associated with developmental changes to the airway or lung structure. These findings suggest that hyperoxia exposure during viral LRTI at young age may aggravate subsequent long-term pulmonary sequelae. Further research is needed to investigate the specific mechanisms underlying this alteration to pulmonary function.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9696792PMC
http://dx.doi.org/10.3390/pathogens11111334DOI Listing

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