Abstract
Simple SummaryEscherichia coli frequently causes bacterial diarrhea in piglets. Vaccine development and improved feeding and animal management strategies have reduced the incidence of bacterial diarrhea in piglets to some extent. However, current breeding strategies also have the potential to improve piglet resistance to diarrhea at a genetic level. This study sought to advance the current understanding of the functional and regulatory mechanisms whereby the candidate gene bactericidal/permeability-increasing protein (BPI) regulates piglet diarrhea at the cellular level.The efficacy and regulatory activity of bactericidal/permeability-increasing protein (BPI) as a mediator of Escherichia coli (E. coli) F18 resistance remains to be defined. In the present study, we evaluated lipopolysaccharide (LPS)-induced changes in BPI gene expression in porcine kidney (PK15) cells in response to E. coli F18 exposure. We additionally generated PK15 cells that overexpressed BPI 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 BPI expression rose significantly following LPS exposure in response to E. coli F18ac stimulation (p < 0.01). Colony count assays and qPCR analyses revealed that E. coli F18 adherence to PK15 cells was markedly suppressed following BPI overexpression (p < 0.01). BPI overexpression had no significant effect on the mRNA-level expression of genes associated with glycosphingolipid biosynthesis or TLR4 signaling. BPI overexpression suppressed the LPS-induced TLR4 signaling pathway-related expression of proinflammatory cytokines (IFN-α, IFN-β, MIP-1α, MIP-1β and IL-6). Overall, our study serves as an overview of the association between BPI and resistance to E. coli F18 at the cellular level, offering a framework for future investigations of the mechanisms whereby piglets are able to resist E. coli F18 infection.
Highlights
Bactericidal/permeability-increasing protein (BPI) is expressed at high levels in a range of animal cell and tissue types, with pronounced expression being evident in neutrophils [1,2]
We found that BPI overexpression did not impact Toll-like receptor 4 (TLR4), CD14, TNF-α, IL-1β, MyD88, FUT1 or FUT2 expression (p > 0.05)
We found that MyD88, FUT1 and FUT2 were highly expressed in PK15 cells (Figure 4)
Summary
Bactericidal/permeability-increasing protein (BPI) is expressed at high levels in a range of animal cell and tissue types, with pronounced expression being evident in neutrophils [1,2]. The BPI family proteins BPIFA1 and BPIFB1 exhibit antimicrobial and LPS-neutralizing activity, and there is experimental evidence for their roles in nasopharyngeal carcinoma and other respiratory diseases [8,9,10,11].
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