The Impact of Expression on F18 Infection in Porcine Kidney Cells.

The efficacy and regulatory activity of bactericidal/permeability-increasing protein () as a mediator of () F18 resistance remains to be defined. In the present study, we evaluated lipopolysaccharide (LPS)-induced changes in gene expression in porcine kidney (PK15) cells in response to F18 exposure. We additionally generated PK15 cells that overexpressed to assess the impact of this gene on Toll-like receptor 4 (TLR4) signaling and glycosphingolipid biosynthesis-related genes. Through these analyses, we found that expression rose significantly following LPS exposure in response to F18ac stimulation ( < 0.01). Colony count assays and qPCR analyses revealed that F18 adherence to PK15 cells was markedly suppressed following overexpression ( < 0.01). overexpression had no significant effect on the mRNA-level expression of genes associated with glycosphingolipid biosynthesis or TLR4 signaling. overexpression suppressed the LPS-induced TLR4 signaling pathway-related expression of proinflammatory cytokines (, , , and ). Overall, our study serves as an overview of the association between and resistance to F18 at the cellular level, offering a framework for future investigations of the mechanisms whereby piglets are able to resist F18 infection.