NF-κB-Dependent Snail Expression Promotes Epithelial-Mesenchymal Transition in Mastitis

Area of Science:

• Veterinary Medicine
• Cell Biology
• Molecular Biology

Background:

• Mastitis is a prevalent ruminant disease potentially leading to inflammatory fibrosis.
• Fibrosis is often linked to epithelial-mesenchymal transition (EMT), but the mechanisms in mastitis are unclear.
• Nuclear factor kappa-B (NF-κB) and Snail are known EMT regulators.

Purpose of the Study:

• To elucidate the molecular mechanisms of mastitis-induced fibrosis.
• To investigate the role of the Toll-like receptor 4 (TLR4)/NF-κB/Snail pathway in mastitis-associated EMT.

Main Methods:

• Primary goat mammary epithelial cells (GMECs) were treated with lipopolysaccharide (LPS) to simulate mastitis.
• Analyzed cellular morphology, mesenchymal marker expression, and signaling pathway activation.
• Investigated the effect of Snail knockdown and TLR4/NF-κB pathway inhibition.

Main Results:

• LPS treatment induced mesenchymal transformation and marker expression in GMECs.
• Snail expression was upregulated by LPS and suppressed by inhibiting the TLR4/NF-κB pathway.
• Snail knockdown reduced LPS-induced EMT and modulated inflammatory cytokine expression.
• Key molecules of the TLR4/NF-κB/Snail pathway were elevated in mastitis tissues.

Conclusions:

• Snail is a critical mediator of LPS-induced EMT in goat mammary epithelial cells.
• The TLR4/NF-κB/Snail signaling pathway is essential for mastitis-induced fibrosis.
• Targeting this pathway may offer therapeutic strategies for mastitis complications.