Impact of cadmium exposure on swine enterocytes

• Published in: Toxicology letters Vol. 287; pp. 92 - 99
• Main Authors: Razzuoli, E., Mignone, G., Lazzara, F., Vencia, W., Ferraris, M., Masiello, L., Vivaldi, B., Ferrari, A., Bozzetta, E., Amadori, M.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01-05-2018
• Subjects: Cd2; IFN-β; IL-8; Inflammation; IPEC-J2; Salmonella typhimurium; Cd2; Inflammation; IFN-β; IL-8; Salmonella typhimurium; IPEC-J2
• ISSN: 0378-4274; 1879-3169
• DOI: 10.1016/j.toxlet.2018.02.005

•IPEC-J2 cells are suited to mimic interactions between host and Cadmium.•IPEC-J2 cells can uptake Cadmium.•Low and moderate Cadmium concentration perform different effects.•Cadmium performs pro-inflammatory effects and reduction of cell viability.
We tested cadmium (Cd2+) effects on porcine IPEC-J2 cells, which represent an in vitro model of the interaction between intestinal cells and both infectious and non-infectious stressors. Accordingly, we investigated the effects of low (2 μM) to moderate (20 μM) concentrations of Cd2+, in terms of pro-inflammatory gene expression and protein release, as well as of infectivity in a Salmonella typhimurium penetration model. Our data showed a significant (P < .001) increase of intracellular Cd2+ after 3, 6 and 24 h of exposure with respect to levels at 1 h. These data showed the ability of IPEC-J2 to absorb Cd2+ as a function of both time and concentration. Also, the absorption of this heavy metal was related to a significant modulation of important pro-inflammatory messengers. In particular, down-regulation of IL-8 was associated with a significant decrease of Salmonella typhimurium ability to penetrate into IPEC-J2 cells, in agreement with a previous study in which an anti-IL 8 antibody could significantly inhibit Salmonella penetration into the same cells (Razzuoli et al., 2017). This finding demonstrates the ability of Cd2+ to affect the outcome of an important host-pathogen relationship. In conclusion, our study highlighted the ability of an environmental pollutant like Cd2+ to modulate innate immune responses in terms of chemokine release and gene expression, and susceptibility to microbial infections.