Endoplasmic reticulum (ER) stress occurs when proteins misfold during biosynthesis in the ER. ER stress in intestinal secretory cells has been implicated in the aetiology of inflammatory bowel diseases (IBD) and intestinal inflammation in mice. Intestinal secretory cells are susceptible to ER stress due to high rates of protein synthesis, and ER stress in these cells results in reduced production of cell surface and secreted proteins leading to thinner mucus with a lower anti-microbial content, allowing penetration by luminal microbes, leading to inflammation. Cells experiencing ER stress attempt to restore homeostasis via the unfolded protein response (UPR), which enables the cells to increase the protein folding capacity of the ER. The primary focus of this thesis is to examine whether the drugs that are efficacious in IBD treatment modulate goblet cell function and ER homeostasis, and whether drugs that modulate ER stress can suppress intestinal inflammation and restore intestinal homeostasis.