# Dysregulated interferon signaling and hyperinflammation upon FCGBP knockdown in goat bronchial epithelial cells infected with Pasteurella multocida

## TL;DR

This study shows that reducing FCGBP in goat lung cells leads to overactive immune responses and inflammation when infected with a common respiratory pathogen.

## Contribution

The novel contribution is identifying FCGBP's role in modulating immune signaling and preventing hyperinflammation during P. multocida infection in goats.

## Key findings

- FCGBP knockdown disrupts cellular barrier function in goat bronchial epithelial cells.
- Reduced FCGBP leads to overactivation of interferon and inflammatory signaling pathways upon infection.
- Key immune pathways like HIF-1, TNF, and NOD-like receptor are dysregulated in FCGBP-deficient cells.

## Abstract

The Fc gamma binding protein (FCGBP) is pivotal for mucosal immune defense against Pasteurella multocida (P. multocida), a key pathogen that induces respiratory ailments in ruminants. However, the mechanism by which FCGBP modulates the pulmonary immune response following infection remains unclear.

This study investigated the role of FCGBP in the immune response of goat bronchial epithelial cells against P. multocida infection. An in vitro infection model was established using FCGBP-knockdown goat bronchial epithelial cells infected with P. multocida serotype 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).

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 P. multocida. These findings offer a foundational framework for elucidating the immune function of FCGBP in goat bronchial epithelial cells infected with P. multocida.