Respiratory syncytial virus infection differentiates airway dysfunction in the central and peripheral airways in OVA-sensitized mice.

Much evidence suggests that respiratory syncytial virus (RSV) infection prolongs airway hyperresponsiveness (AHR) and exacerbates asthma by enhancing airway inflammation. However, the characteristic of airway inflammation and kinetics of airway dysfunction occurred in the central and peripheral airways were not fully delineated. The objective of this study was to investigate the effect of RSV on the allergic airway inflammation in different size airways and to elucidate its possible mechanism.

Inhibition of CD8+ T lymphocytes attenuates respiratory syncytial virus-enhanced allergic inflammation.

Background: CD8+ T cells have an important role in the pathogenesis of respiratory virus-induced asthma exacerbations. However, the cellular mechanism of CD8+ T cells, linking viral respiratory infections to the development of airway inflammation, is not well defined.

Objectives: To clarify the role of CD8+ T cells in the development of respiratory virus-induced asthma exacerbations.

[Reproduction of severe asthma model in mice].

Objective: To reproduce a severe asthma model in ovalbumin (OVA)-sensitized Balb/C mice by induction with respiratory syncytial virus (RSV).

Methods: Thirty Balb/C mice were randomly divided into phosphate buffer solution (PBS) control group, OVA group and OVA/RSV group. The severe asthma model was reproduced by sensitization with intraperitoneal injection of OVA, followed by repeated inhalation of OVA combined with repeated intranasal instillation of RSV (1.