From the current state-of-the-art, it is clear that nanotechnology applications are expected to bring a range of benefits to the food sector aiming at providing better quality and conservation. In the meantime, a growing number of studies indicate that the exposure to certain engineered nanomaterials (ENMs) has a potential to lead to health complications and that there is a need for further investigations in order to unravel the biological outcomes of nanofood consumption. In the current review, we summarize the existing data on the (potential) use of ENMs in the food industry, information on the toxicity profiles of the commonly applied ENMs, such as metal (oxide) nanoparticles (NPs), address the potential food safety implications and health hazards connected with the consumption of nanofood. A number of health complications connected with the human exposure to ENMs are discussed, demonstrating that there is a real basis for the arisen concern not only connected with the gut health, but also with the potency to lead to systemic toxicity. The toxicological nature of hazard, exposure levels and risk to consumers from nanotechnology-derived food are on the earliest stage of investigation and this review also highlights the major gaps that need further research and regulation.

Recent studies support beneficial effects of polyphenols in various chronic inflammatory diseases, for example, the inflammatory bowel diseases. Inhibition of NF-κB activation by polyphenols could explain part of their anti-inflammatory properties, but few data are available on the intestine. The purpose of the present study was thus to investigate the effects of some polyphenols on NF-κB activation using human intestinal Caco-2 cells. Effects of standard polyphenols (50 μmol/l) were studied on different cellular events associated with NF-κB activation: (i) NF-κB activity using cells transiently transfected with a NF-κB–luciferase construct and stimulated by inflammatory agents (IL-1β, TNF-α or lipopolysaccharides (LPS)); (ii) phosphorylation of the inhibitor of κB (IκB-α) analysed by Western blot; (iii) secretion of IL-8 quantified by ELISA assay. Results showed that chrysin and ellagic acid inhibited NF-κB activity, whereas genistein and resveratrol increased it. These effects were independent of the nature of the inducer, indicating that polyphenols may modulate NF-κB activation by acting on a common event to the cytokine- and LPS-mediated cascades. Chrysin strongly reduced (2·5-fold) IL-1β-induced IκB-α phosphorylation, whereas ellagic acid increased it (1·7-fold). Ellagic acid, genistein and epigallocatechin gallate reduced (4- to 8-fold) IL-1β-induced IL-8 secretion, while resveratrol promoted (1·7-fold) the secretion. Chrysin also diminished IL-8 secretion by 1·6-fold (but P>0·05). The data indicate that polyphenols can modulate the NF-κB activation pathway in the intestine. Chrysin could block NF-κB activation via the inhibition of IκB-α phosphorylation. The other molecular targets of the active polyphenols are still to be identified.

The increasing commercial use of silver nanoparticles (Ag-NPs) will inevitably lead to elevated silver exposure and thus to potential human health complications. In this study the acute toxicity of Ag-NPs <20 nm alone and upon co-administration with food matrix component phenolic compounds (PCs) on the cell-based models of the gastrointestinal tract was investigated. An improved co-culture model of Caco-2 and RajiB cells was applied for more precise in vitro simulation of the gastrointestinal tract. The involvement of two major factors contributing to the toxicity of Ag-NPs, i.e. the release of Ag⁺ and the induction of oxidative stress, was investigated. Ag-NPs were cytotoxic for Caco-2 cells with an EC₅₀ of ca. 40 µg/ml. Ag-NPs led to oxidative stress starting from ca. 45 µg/ml. The epithelial barrier integrity disruption by Ag-NPs on Caco-2 cell mono- and co-cultures was established by decreased transepithelial electrical resistances and increased passages of Lucifer Yellow, a paracellular marker. Immunofluorescence staining demonstrated that Ag-NPs affect occludin and zonula occludens 1 distributions, suggesting the opening of tight junctions. Ag⁺, corresponding to the release from Ag-NPs, demonstrated a partial contribution in the toxic parameters, induced by Ag-NPs. Two PCs, quercetin and kaempferol, partially protected the Caco-2 cells from Ag-NP-induced toxicity and maintained the epithelial barrier integrity, disrupted by NPs. No protective effect was observed for resveratrol. The protective effect could be beneficial and decrease the potential toxicity of ingested Ag-NPs. However, the precise mechanisms of barrier-integrity-destabilising action of Ag-NPs/Ag⁺ and protective effect of PCs still require further elucidation.

This study aimed at evaluating the anti-inflammatory properties of a pomegranate fruit husk (PomH) polyphenolic extract, rich in punicalagin, using Caco-2 cells, an in vitro model of human intestinal epithelium. Differentiated cells in bicameral inserts were pretreated or not with a PomH extract or punicalagin, as reference, at the apical side, representing the intestinal lumen. Inflammation was then induced with a cocktail of cytokines (Il-1β, TNFα and IFNγ) and LPS. After 24 h incubation, 3 pro-inflammatory markers, i.e., interleukin (IL)-6, IL-8 and monocyte chemoattractant protein (MCP)-1, were assayed both at their gene transcription (qRT-PCR) and secretion (ELISA) levels. As previously described, the pro-inflammatory cocktail significantly stimulated these 3 markers, at the gene transcript and secretion levels. In inflamed cells, a significant down-regulation of the transcription of the genes encoding IL-6 and MCP-1 was observed in the presence of the PomH extract or punicalagin, while IL-8 transcription was unaffected. Both treatments also decreased the amounts of the 3 proteins with dose-response effects, but only in the apical compartment. A lowered ELISA response was also observed when either IL-6, IL-8 or MCP-1 were mixed with punicalagin in a cell-free culture medium, indicating a direct molecular interaction. In conclusion, the punicalagin-rich PomH extract tested showed anti-inflammatory properties in the Caco-2 in vitro intestinal model. It acted both on the pro-inflammatory gene transcription and protein levels, the later phenomenon being possibly due to a direct molecular trapping. These data suggest that pomegranate husk could be an interesting natural source contributing to prevent intestinal chronic inflammation.