Neonatal antigen and viral exposure alters airway and parenchymal responsiveness in adult mice

<p>Epidemiological data suggests a link between viral infection early in life and long-term symptoms of asthma. We aimed to determine if viral infection in early life exacerbates allergen induced lung hyperresponsiveness (HR) later in life.</p> <p><strong>Methods</strong>: BALB/c mice were exposed to OVA (5 mL 2 mg/mL or saline i.n.) on d0 then inoculated d7 with Influenza A Mem/1/71(H3N1) (10 mL 103.8 pfu or media). Mice were boosted at 4 wks then challenged with 6 aerosols at 8 wks (OVA or saline). AHR was assessed to inhaled MCh (0.1–30 mg/mL) 24 hrs after the final aerosol using a small animal ventilator and a modification of the forced oscillation technique. The Constant Phase Model was fitted to Respiratory Impedance (Zrs) data to produce airway (Raw) and tissue parameters (G, tissue damping; H, tissue elastance).</p> <p><strong>Results:</strong> Both neonatal exposure to Flu (Raw, p = 0.017; H, p < 0.001) and antigen (Raw, p = 0.008; H, p = 0.003) individually induced HR in adult mice. However, there was neither an additive or synergistic effect of the two exposures (Raw, p = 0.531, H, p = 0.311).</p> <p><strong>Conclusions:</strong> These findings demonstrate that exposure to Influenza A virus or OVA during the neonatal period alter lung mechanics when challenged with MCh in adult mice. The addition of viral infection in early life did not exacerbate allergen induced HR.</p>