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Cytokine response after stimulation of culture cells by zinc and probiotic strain.

Miroslava Anna ŠefcováMartin LevkutKatarína BobíkováViera KaraffováViera RevajováIvana Cingeľová MaruščákováMária LevkutováZuzana ŠevčíkováRóbert HerichMikuláš Levkut
Published in: In vitro cellular & developmental biology. Animal (2019)
Intestinal porcine epithelial cells were used for an in vitro analysis of mRNA expression levels of inflammatory cytokines (IL-8, IL-18) and transcriptional factors (MyD88 and NF-κβ). Cells were exposed to inorganic and organic zinc sources (in two different concentrations-50 μmol/L and 100 μmol/L) alone or combined with Lactobacillus reuteri B6/1, which was also applied individually. The total exposure time was 4 h. Quantitative reverse transcriptase PCR was used to determine expression levels of the aforementioned parameters. In general, upregulation was observed; however, a decrease of some mRNA's abundance was also determined. Differences in expression were analysed statistically using ANOVA and Tukey analyses. High relative expression was shown for IL-8, IL-18 and MyD88 in groups treated with 100 μmol/L of inorganic sources of zinc (ZnSO4) (p < 0.05), while groups treated with the organic form did not exhibit significant changes in expression. Also, 50 μmol/L of either zinc source did not significantly modify the transcriptional profile of the cytokines and transcription factors, showing that even inorganic sources, at lower concentrations, do not elicit a significant inflammatory reaction. In summary, supplementation of organic zinc source (Gly-Zn chelate) ensures that IL-8, IL-18, MyD88 and NF-κβ expression levels are not positively regulated. In contrast, inorganic sources of zinc (ZnSO4) could induce an inflammatory reaction. However, this response could be dampened if L. reuteri B6/1 is administered, showing the helpful aspect of using probiotics to modulate an inflammatory response. Conclusively, the use Gly-Zn chelate appears as an optimal alternative for Zn administration that does not compromise normal intestinal homeostasis.
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