CCN1 is well studied in terms of its functions in injury repair, cell adhesion survival and apoptosis, bacterial clearance and mediation of inflammation-related pathways, such as the TLR2/4 pathways. However, the role of CCN1 protein and its interaction with TLR2/4 pathways in intestinal epithelial cells was not elucidated after Listeria monocytogenes infection. The results of this study confirm that L. monocytogenes infection induced intestinal inflammation and increased the protein expression of CCN1, TLR2, TLR4 and p38, which followed a similar tendency in the expression of genes related to the TLR2/4 pathways. In addition, organoids infected by L. monocytogenes showed a significant increase in the expression of CCN1 and the activation of TLR2/4 pathways. Furthermore, pre-treatment with CCN1 protein to organoids infected by L. monocytogenes could increase the related genes of TLR2/4 pathways and up-regulate the expression of TNF, and increase the count of pathogens in organoids, which indicates that the interaction between the CCN1 protein and TLR2/4 signaling pathways in intestinal epithelial cells occurred after L. monocytogenes infection. This study will provide a novel insight of the role of CCN1 protein after L. monocytogenes infection in the intestine.
Keywords: CCN1; Listeria monocytogenes; TLR2/4 pathways; intestine epithelial cells.