Calycosin ameliorates airway inflammatory injury induced by respiratory syncytial virus via inhibiting NLRP3 inflammasome activation in mice.

Abstract

Respiratory syncytial virus (RSV) is a predominant pathogen inducing respiratory tract infections among infants and elderly. Calycosin exhibits antiviral properties, yet its efficacy against RSV has not been elucidated. In this study, cyclophosphamide was administered to induce immune deficiency in adult mice, following which RSV was introduced via the intranasal route to establish an RSV infection model in mice. The viral load in lung tissue, airway resistance, inflammatory cell quantity and pro-inflammatory factor levels within bronchoalveolar lavage fluid (BALF) were quantified. Pathological changes were examined and the NOD-like receptor protein 3 (NLRP3) inflammasome activation status was assessed in lung tissue. The results demonstrated that Calycosin treatment markedly decreased the RSV viral load inside lung tissue, decreased inflammatory factor quantity and pro-inflammatory factor levels within BALF, and alleviated airway resistance, inflammatory injury, as well as goblet cell hyperplasia of mouse lung tissue. Notably, Calycosin significantly suppressed NLRP3 inflammasome activation inside RSV-infected mouse lung tissue. However, co-treatment with Nigericin diminished the protective effects of Calycosin on airway inflammatory injury in RSV-infected mice. These findings indicate that Calycosin alleviates airway injury induced by RSV infection, and the underlying mechanism is associated with the inhibition of the inflammatory response mediated by NLRP3 inflammasome activation.