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ZnO protects human intestinal Caco-2 cells from the damage induced by enterotoxigenic E. coli (ETEC)

There is some evidence that zinc oxide (ZnO) is able to protect against intestinal diseases. Despite the suggestions of some studies that ZnO may have antibacterial activity, mechanisms of ZnO protective effect have not yet been elucidated. The potential benefits of ZnO against the damages induced by enterotoxigenic Escherichia coli (ETEC) strain K88 on Caco-2 cells and the mechanisms related have been investigated.

Cell permeability, measured as transepithelial electrical resistance (TEER) and 14C-inulin transfer, was unchanged by 0.01 and 1 mM ZnO treatments and moderately increased with 5 mM ZnO, as compared to untreated cells. ETEC (1 x 108 CFU/ml) was able to induce a TEER decrease and a 14C-inulin transfer increase after 2.5 h of infection in Caco-2 cells. Treatment with ETEC together with ZnO (already with 0.2 mM) prevented membrane integrity disruption. ETEC was able to adhere to enterocytes and, to some extent, to invade the cells.

ZnO reduced bacterial adhesion and blocked invasively, in a dose dependent manner. ETEC infection upregulated the expression of pro-inflammatory cytokines interleukin (IL)-8, growth-related oncogene (GRO)-a and tumour necrosis factor (TNF)-a, and reduced that of anti-inflammatory cytokine transforming growth factor-b, as compared to uninfected cells. Addition of ZnO (0.2 or 1 mM) counteracted the alterations on cytokine mRNA levels caused by ETEC.

The protective effects of ZnO were not due to an antibacterial activity of ZnO, since the viability of ETEC grown in ZnO containing medium was unaffected. In conclusions, ZnO may protect intestinal cells against ETEC infection by inhibiting adhesion and internalisation of bacteria, preventing increase of tight junction permeability and modulating cytokine gene expressions.

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