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 () virulent strains. However, the role of lipooligosaccharide sialylation modification in the process of infection and penetration of the porcine respiratory epithelial barrier is still unclear. In this study, we investigated the role and mechanism of -mediated lipooligosaccharide sialylation in invasion of the host respiratory epithelial barrier. Specifically, -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 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 which will contribute to better prevention and control of infection in piglets.

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http://dx.doi.org/10.1021/acsinfecdis.0c00850DOI Listing

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