{'fraction_non_alphanumeric': 0.03515625, 'fraction_numerical': 0.02109375, 'mean_word_length': 5.1291866028708135, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Respiratory Syncytial Virus Inhibits Epithelial Na+ Currents by Upregulating iNOS

We have shown respiratory syncytial virus (RSV) infection of BALB/c mice resulted in a 40% reduction in Na+ driven alveolar fluid clearance (AFC), here we investigated the possible roles of iNOS and NO in this inhibition. H441 cells were infected with a GFP tagged RSV, whole‐cell and single channel Na+ currents were recorded 3 to 5 days after infection. RSV infection significantly decreased whole‐cell total and amiloride‐sensitive Na+ current in GFP (+) infected cells to 59% and 12% of those of the control uninfected cells; 4 pS ENaC single‐channel NPo was also decreased from 0.48 to 0.10. iNOS was significantly upregulated and nitrite concentration was 41% higher in RSV infected cells. Nuclear translocation of NF‐kB p65 subunit and NF‐kB activation were also upregulated. None of these effects were seen in cells exposed to UV‐inactivated RSV. Knock‐down of NF‐kB reversed the upregulation of iNOS, meanwhile inhibition of NO production with 1um 1400W partially restored amiloride‐sensitive currents in GFP (+) cells. These data indicate RSV infection inhibits Na+ currents via upregulation of iNOS and NO; provide new insight into the mechanisms of RSV induced decrease of AFC in vivo.