Knockdown of the Autophagy Protein Beclin-1 Does Not Affect Innate Cytokine Production in Human Lung Epithelial Cells during Respiratory Syncytial Virus Infection.

Abstract

Listen

Translate article

Respiratory syncytial virus (RSV) is a major cause of respiratory tract infections in young children, globally. Autophagy is a cellular degradation process that mediates cell survival. Studies using mouse models have demonstrated that inhibiting autophagy affects the production of cytokines triggered by RSV. However, the effect of autophagy on RSV-induced cytokine production in human cells remains inadequately studied. Our previous research showed that inhibiting autophagy using pharmacological inhibitors did not affect the innate cytokine production in human lung epithelial cells (BEAS-2B) following RSV infection. In this study, we sought to validate these findings using a more specific approach, employing short-interfering RNA (siRNA) to target the important autophagy protein Beclin-1 (Bec-1). Prior to measuring cytokine production, we confirmed that silencing Bec-1 with siRNA effectively suppressed autophagy without affecting cell viability. Our results revealed that inhibiting autophagy through Bec-1 knockdown did not affect the production of innate cytokines CXCL8 and CCL5 in BEAS-2B cells during RSV infection, consistent with our previous findings using pharmacological inhibitors. Overall, our data suggest that targeting autophagy may not be an effective strategy for alleviating RSV-induced airway inflammation.