Abstract
Epithelial cells (enterocytes) form part of the intestinal barrier, the largest human interface between the internal and external environments, and responsible for maintaining regulated intestinal absorption and immunological control. Under inflammatory conditions, the intestinal barrier and its component enterocytes become inflamed, leading to changes in barrier histology, permeability, and chemical mediator production. Omega-3 (ω-3) polyunsaturated fatty acids (PUFAs) can influence the inflammatory state of a range of cell types, including endothelial cells, monocytes, and macrophages. This review aims to assess the current literature detailing the effects of ω-3 PUFAs on epithelial cells. Marine-derived ω-3 PUFAs, eicosapentaenoic acid and docosahexaenoic acid, as well as plant-derived alpha-linolenic acid, are incorporated into intestinal epithelial cell membranes, prevent changes to epithelial permeability, inhibit the production of pro-inflammatory cytokines and eicosanoids and induce the production of anti-inflammatory eicosanoids and docosanoids. Altered inflammatory markers have been attributed to changes in activity and/or expression of proteins involved in inflammatory signalling including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), peroxisome proliferator activated receptor (PPAR) α and γ, G-protein coupled receptor (GPR) 120 and cyclooxygenase (COX)-2. Effective doses for each ω-3 PUFA are difficult to determine due to inconsistencies in dose and time of exposure between different in vitro models and between in vivo and in vitro models. Further research is needed to determine the anti-inflammatory potential of less-studied ω-3 PUFAs, including docosapentaenoic acid and stearidonic acid.
Highlights
In humans, the gut barrier is the largest interface separating the internal and external environments
Disruption of intestinal epithelium function leads to increased permeability and loss of immunological control, which is believed to contribute to a number of pathological states and diseases, including inflammatory bowel diseases (Crohn’s disease and ulcerative colitis), coeliac disease and irritable bowel syndrome [2]
Communication between epithelial cells, the gut microbiota, and intestinal immune cells is through both direct cell–cell contact and through the production of chemical mediators, including both small metabolites such as short-chain fatty acids (SCFAs) and larger immune mediators such as cytokines and chemokines [3,4]
Summary
The gut (intestinal) barrier is the largest interface separating the internal and external environments. Human colorectal tumour-derived cell lines, such as Caco-2, T84, and HT-29, as well as rodent-derived cell lines, such as IEC-6 and IEC-18, provide replicable and high-throughput models of the intestinal epithelium [20,21], whilst organ-on-a-chip cultures have begun to replicate more in vivo-like epithelial properties and behaviours [22] These models allow for in vitro assessment of a multitude of outcomes, including changes to membrane composition, permeability, transport processes, inflammatory mediator production, receptors and signalling pathways, the cell cycle and apoptosis. This was not seen in T84 cells where DHA supplementation decreased DPA content [25]
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