Pathogens
utilize various mechanisms to escape host immunological
surveillance, break down different tissue barriers, and cause infection.
Sialylation is an important surface modification of bacterial outer
membrane components, especially the lipooligosaccharide of Gram-negative
bacteria. It is widely involved in multiple microbe–host interactions,
such as bacterial virulence regulation, host recognition, and immune
evasion. There are some sialylation modifications on the lipooligosaccharide
structure of Glaesserella parasuis (G. parasuis) virulent strains. However, the role of lipooligosaccharide sialylation
modification in the process of G. parasuis infection
and penetration of the porcine respiratory epithelial barrier is still
unclear. In this study, we investigated the role and mechanism of lsgB-mediated lipooligosaccharide sialylation in G. parasuis invasion of the host respiratory epithelial
barrier. Specifically, G. parasuis lsgB-mediated
lipooligosaccharide sialylation and sialylated-lipooligosaccharide
interacted with Siglec1 on porcine alveolar macrophages 3D4/21 and
triggered the subsequent generation of TGFβ1 through Siglec1/Dap12/Syk/p38
signaling cascade. TGFβ1 decreased the tracheal epithelial tight
junctions and the expression of extracellular adhesion molecule fibronectin,
thus assisting G. parasuis invasion and entry to
the respiratory epithelial barrier. Characterizing the potential effects
and mechanisms of lipooligosaccharide sialylation-mediated TGFβ1
production would further expand our current knowledge on the pathogenesis
of G. parasuis which will contribute to better prevention
and control of G. parasuis infection in piglets.