Tumor necrosis factor-α upregulates polymeric immunoglobulin receptor expression by NF-κB signaling pathways in grass carp (Ctenopharyngodon idellus) liver cells.

ABSTRACT

The polymeric immunoglobulin receptor (pIgR) is essential for controlling polymeric immunoglobulin to defend species from invading pathogens. However, the modulation pathway of pIgR expression in teleosts remains unclear. In this paper, to define that the cytokine TNF-α impacted the expression of pIgR, the recombinant proteins of TNF-α of grass carp were first prepared after approving that natural pIgR was expressed in liver cells of grass carp (Ctenopharyngodon idellus) (L8824). L8824 cells were incubated with variable amounts of recombinant TNF-α at various times, the results revealed that pIgR expressions showed a significant dose-dependent elevation at the gene and proteins, and a similar alteration trend was detected for the pIgR protein (secretory component SC) secreted by L8824 cells into the culture supernatant. Moreover, nuclear factor kappa-B (NF-κB) inhibitors PDTC was used to study whether TNF-α regulated pIgR expressions through the NF-κB signaling pathways. L8824 cells were treated with TNF-α, inhibitor PDTC, and TNF-α + PDTC mixtures, respectively, and the levels of pIgR genes and pIgR protein in cells and SC in the culture supernatant decreased in cells treated with PDTC contrasted to the control, and subjected to reduced expression of PDTC + TNF-α reduced expression contrasted to that treated just with TNF-α, demonstrating that suppression of NF-κB obstructed the ability of TNF-α to elevate pIgR gene and pIgR protein in cells and SC in the culture supernatant. These outcomes indicated that TNF-α raised pIgR gene expression, pIgR protein, and SC creation, and this pIgR expression induced by TNF-α was modulated by complicated pathways that included NF-κB signaling mechanism, confirming TNF-α as a pIgR expression modulator and enhancing a deeper insight of the regulatory pathway for pIgR expression in teleosts.