The Impact of BPI Expression on Escherichia coli F18 Infection in Porcine Kidney Cells.
Jian JinYanjie HuangShouyong SunZhengchang WuShenglong WuZongjun YinWen-Bin BaoPublished in: Animals : an open access journal from MDPI (2020)
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.
Keyphrases
- escherichia coli
- toll like receptor
- inflammatory response
- induced apoptosis
- lps induced
- immune response
- poor prognosis
- gene expression
- cell cycle arrest
- signaling pathway
- nuclear factor
- binding protein
- cell proliferation
- transcription factor
- endoplasmic reticulum stress
- oxidative stress
- long non coding rna
- metabolic syndrome
- anti inflammatory
- klebsiella pneumoniae
- epithelial mesenchymal transition
- weight loss
- cell wall