Background: Severe lower respiratory tract infections in infants and young children are frequently caused by respiratory syncytial virus (RSV), with the degree of illness strongly associated with disproportionate inflammatory activity. The signaling protein A20 (TNFAIP3) functions to inhibit NF-κB pathway activation, suggesting a possible role in tempering RSV-triggered lung inflammation. In this study, we assessed how RSV infection alters A20 gene expression in the lungs using a mouse model system.
Methods: Of the twelve female BALB/c mice allocated for the study, half were administered RSV intranasally at a concentration of 3 × 106 plaque-forming units (PFU), while the remaining six served as uninfected controls. All animals were humanely euthanized five days post-infection. Upon collection, lung tissue samples were immediately processed. The relative expression levels of messenger RNA (mRNA) for the TNFAIP3 gene, which encodes the A20 protein, were subsequently quantified using real-time reverse transcription polymerase chain reaction (RT-PCR).
Results: Analysis by quantitative PCR revealed that A20 expression was significantly higher in the lungs of RSV-infected mice compared with uninfected controls at day 5 post-infection (P = 0.0048).
Conclusion: The upregulation of A20 in RSV-infected mice suggests its potential role in modulating post-viral pulmonary inflammation.
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