IL-13 Modulates Antiviral Effector and Proinflammatory Pathways in Rhinovirus-Infected Pediatric Bronchial...

Area of Science:

• * Immunology
• * Pulmonology
• * Virology

Background:

• * Rhinovirus (RV) frequently triggers asthma exacerbations in children.
• * The role of IL-13-driven T2 inflammation in airway epithelial responses to RV is not well understood.

Purpose of the Study:

• * To investigate how IL-13-mediated T2 inflammation influences the response of pediatric bronchial epithelial cells (BECs) to RV infection.

Main Methods:

• * BECs from children with and without asthma were cultured and pretreated with IL-13 to model T2 inflammation.
• * Cells were infected with RV-A16, and RNA sequencing was performed at multiple time points post-infection.
• * Gene expression patterns were analyzed using linear and generalized additive models with pathway analysis.

Main Results:

• * RV infection and IL-13 stimulation induced significant changes in gene expression.
• * IL-13 pretreatment did not alter RV load or interferon-stimulated genes.
• * IL-13 suppressed specific antiviral effector genes while enhancing inflammatory and cell-death pathways.

Conclusions:

• * IL-13 selectively impairs epithelial antiviral responses and amplifies secondary inflammation during RV infection.
• * These findings offer mechanistic insights into how T2 inflammation contributes to severe outcomes in viral-induced asthma.