Dysregulated interferon signaling and hyperinflammation uponknockdown in goat bronchial epithelial cells infected with.

Abstract

INTRODUCTION: The Fc gamma binding protein (FCGBP) is pivotal for mucosal immune defense against(), a key pathogen that induces respiratory ailments in ruminants. However, the mechanism by which FCGBP modulates the pulmonary immune response following infection remains unclear. METHODS: This study investigated the role of FCGBP in the immune response of goat bronchial epithelial cells againstinfection. An in vitro infection model was established using FCGBP-knockdown goat bronchial epithelial cells infected withserotype D, and transcriptome sequencing coupled with bioinformatics was then used to detect differentially expressed genes (DEGs) and elucidate their regulatory networks. The expression levels of key DEGs and inflammatory factors were subsequently validated via quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). RESULTS AND DISCUSSION: The results indicated that FCGBP maintains homeostasis and provides immune protection in goat lungs. Knockdown of FCGBP in goat bronchial epithelial cells leads to impaired cellular barrier function, resulting in excessive activation of type I interferon, HIF-1, TNF, and NOD-like receptor signaling pathways following infection with. These findings offer a foundational framework for elucidating the immune function of FCGBP in goat bronchial epithelial cells infected with.