The effect of algal polysaccharides laminarin and fucoidan on colonic pathology, cytokine gene expression and Enterobacteriaceae in a dextran sodium sulfate-challenged porcine model

Ulcerative colitis (UC) is a form of inflammatory bowel disease which has increased in incidence in recent years(,1,2). Clinically, UC is associated with bloody diarrhoea, abdominal cramps, weight loss and fatigue(,3). The inflammation pattern typical of UC is confined to the large intestine and is characterised histologically by alterations in the mucosal layer, including compromised epithelial integrity, goblet cell loss and infiltrations of immune cells(,3,4). The aetiology of UC is thought to reflect a failure of the host to achieve immune homeostasis in response to the presence of microbes in the colonic lumen. Features of this immune dysregulation may include excessive production of signalling pro-inflammatory cytokines, which can serve to initiate and perpetuate the chronic inflammatory pattern of UC. This aberrant immune response to the colonic microbiota may be exacerbated by the competitive advantage employed by enteric Enterobacteriaceae which can flourish under such conditions(,5) and may contribute to prolonged inflammation. Recent studies complicate this relationship further, indicating a possible earlier role for Enterobacteriaceae in inducing spontaneous colitis(,6). Therefore, the evidence for environmental and particularly microbial involvement in the genesis, severity and persistence of UC demonstrates the complexity of the disease. The location of UC in the large intestine complicates the application of potential oral preventative and/or therapeutic solutions, which must first navigate the digestive processes of the upper gastrointestinal tract in order to influence the lumen environment. The algal-derived fibres laminarin (LAM), a β(1–3, 1–6)-linked glucan, and fucoidan (FUC), a sulfated fucose polymer, have shown immunomodulatory activity(,7), and improve clinical signs when included in the diet of abruptly weaned piglets(,8), which often undergo a period of gastrointestinal tract inflammation during dietary transition. The bioactivity of dietary LAM and FUC reflect in part the absence of appropriate endogenous host enzymes to hydrolyse these complex polysaccharides, which therefore arrive in the large intestine relatively intact and available for interaction with the lumen environment(,9,10). LAM and FUC demonstrate pleiotropic effects in the porcine large intestine including regulation of gene expression of pro- and anti-inflammatory cytokines relevant to UC, and inhibitory effects on the abundance of colonic Enterobacteriaceae(,8,11,12). These biological effects have been accompanied by improvements in nutrient absorption, body-weight gain and incidence of diarrhoea in piglets(,13,14). Thus, it was postulated that dietary LAM and/or FUC may alleviate the inflammation and underlying biological events which characterise UC. Oral exposure to dextran sodium sulfate (DSS) can induce many signs of UC(,15). The objective of the study was to investigate the preventative role of prior consumption of either LAM and FUC, or a combination of both, on the colonic pathology, inflammatory gene expression and abundance of Enterobacteriaceae following a DSS challenge in pigs.